





.i^'^i^')^#^ 



Wmrir 








Class __u_[l_ll_5 
Book 






G)pyright}^'^ 



CDPXRIGHT DEPOSIT. 



DISEASES OF DOMESTICATED BIRDS 



^^^^ 

THE MACMILLAN COMPAKY 

NEW YORK • BOSTON • CHICAGO • DALLAS 
ATLANTA • SAN FRANCISCO 

MACMILLAN & CO., Limited 

LONDON • BOMBAY • CALCUTTA 
MELBOURNE 

THE MACMILLAN CO. OF CANADA, Ltd. 

TORONTO 



^ DISEASES 

OF DOMESTICATED BIRDS 



BY 
ARCHIBALD ROBINSON WARD, B.S.A.. D.V.M. 

Director, Research Department, The Jensen-S^lsbcry 
Laboratories, Kansas City, Missouri 

AND 

BERNARD A. GALLAGHER, D.V.M. 

Bacteriologist. Bureau of Animal Industry, United States 
Department of Agriculture, Washington, D. C. 



WITH INTRODUCTION BY 

VERANUS ALVA MOORE, B.S., M.D., V.M.D. 

Professor of Comparative Pathology, Bacteriology and Meat Inspection, 

New York State Veterinary College at Cornell University, 

and Director of the College 



s^txo gotfe 

THE MACMILLAN COMPANY 
1920 

All rights reserved 






Copyright, 1920, 
By the MACMILLAN COMPANY 



Set up and electrotyped. Published, January, 1920 



n^ -3 1920 



©CI.A559G85 



^x^ 



" 1 



PEEFACE 

The writing of this book has been prompted by a conviction held 
by the authors, regarding the magnitude of the losses experienced 
by poultry producers as a result of preventable infectious diseases 
and parasitic infestations. 

It is believed that the importance of these losses warrants the 
effort expended in presenting the essential facts concerning poultry 
diseases to meet the needs of veterinary practitioners, veterinary stu- 
dents and poultrjTuen. 

The title of the book indicates a slight broadening of scope beyond 
the field of a work on diseases of poultry. Material included deals 
with the ostrich, cage birds and wild birds in semi-domestication in 
zoological gardens. Chapters dealing with anatomy of birds, and 
killing of poultry have been included. 

The peculiarities of diseases of birds are indicated by the emphasis 
laid on certain features of the subject matter. In general, skill in 
diagnosing diseases of birds by observing symptoms is of less impor- 
tance than ability to recognize the identity of disease at autopsy. 
Symptoms are slightly characteristic, but autopsy material is freely 
available. Consequently more facts concerning details of gross 
lesions are given than those relating to symptoms. In many cases, 
particularly in the septicemias, symptoms and lesions are not dis- 
tinctive, and fine distinctions of etiology must be made by a bacteri- 
ologist. On this account considerable material useful to a bacteri- 
ologist alone has been included. 

Available sources of information are indicated in the references 
appended to each chapter and by specific references to authors in the 
text. Special acknowledgment is made for assistance obtained from 
IsTeumann's " Parasites et Maladies Parasitaires des Oiseaux Do- 
mestiques " in the preparation of the chapters on parasites. Much 
material concerning the less common parasites has been dravni from 
this book and l^eumann's zoological nomenclature has been largely 
followed. s, \ ^ 

A. R. W. 

B. A. G. 



introductio:n' 

The statement is accepted that diseases are the greatest hindrance 
to the development of animal and poultry husbandry. Measures 
for the prevention, successful treatment or control of these maladies 
must come from those who understand their nature. It is grati- 
fying, therefore, that veterinarians, and others interested in the 
subject, are to have access to a volume dealing with the diseases 
of poultry, prepared by men of long experience in the study of the 
phenomena of disease. Likewise, poultry raisers will appreciate 
a treatise setting forth the known facts concerning the maladies 
which sooner or later may affect their flocks. A book of this kind 
will be of indispensable value in eliminating many of the miscon- 
ceptions regarding the diseases of poultry and in pointing out the 
things that are known and the precautions that must be observed in 
maintaining healthy flocks. 

The extent of the poultry industry in the United States is little 
appreciated by veterinarians. There is no other species in the 
animal kingdom that contributes to the material support of so large 
a number of people as the domesticated fowl. In addition turkeys, 
geese, ducks and pigeons are significant factors in food production 
while the ostrich and other birds play an important part in orna- 
mentation. In the Hartz Mountains, the raising of canary birds for 
the amusement and entertainment of people is an important in- 
dustry. 

The barnyard fowl plays a large part in the food supply of the 
country. The extent of the poultry business can be approximated 
from the fact that in 1910 there were 5,578,525 farms in the United 
States that reported a total of 280,350,000 fowls with a value of 
$140,205,000. With the prices at the present time, their value 
would be treble that of 1910. In 1915, the United States exported 
20,784,000 dozen eggs but it imported over 3,000,000 dozen and 
over 8,000,000 pounds of egg yolks and frozen eggs. These figures 
indicate the large number of people who are financially interested 
in the poultry business. 

The raising of turkeys and other species is also sig-nificant. In 
1910 there were in the United States 3,688,000 turkeys with a value 



viii mTEODUCTION 

of $6,605,000; 2,906,000 ducks valued at $1,567,000; 4,431,000 
geese valued at $3,194,000 ; 1,765,000 guinea fowls valued at 
$613,000 ; 2,730,000 pigeons with a value of $762,000 ; 6,458 pea 
fowls estimated at $18,000 ; and 5,361 ostriches valued at $1,- 
696,000, In 1915, this country imported ostrich and other feathers 
to the value of $2,500,000. Besides, there is a large business in 
song and other birds maintained as pets. 

In certain localities, the raising of one or more species of poultry- 
constitutes the essential occupation of many of the people. The pro- 
ductivity of domestic fowls is greater than that of any other species 
of animals in proportion to their value. The price of the annual 
products from a flock of ducks, hens or turkeys may be many times 
larger than the cost of the original flock. 

There is no other form of animal life that suffers more from the 
ravages of disease than fowls. The losses from the general maladies 
are heavy and those from the infectious ones are sometimes appal- 
ling. Various estimates have been made of the annual losses occa- 
sioned by these causes. They vary from 10 to 30 per cent. Hens 
in particular suffer from a wide range of diseases and parasitisms. 
Some of these are veritable plagues and at times are the cause of 
serious losses. In 1903, while studying poultry diseases in a lo- 
cality where eggs and chickens were the cliief articles of commerce, 
it was not unusual to learn of individual losses ranging from a few 
hundred to several thousand dollars due to roup or diphtheria. 
Other large flocks were decimated by tuberculosis. While it is easy 
to understand that heavy losses may occur in localities where fowls 
are kept in large numbers, it should be recognized that they are 
proportionately heavy in smaller flocks. In such circumstances, the 
death of a few hens is often the cause of much privation if not actual 
suffering among their owners who are dependent upon the products 
of their fowls for the necessities of life. 

The general diseases of poultry present many points of interest, 
although they have received relatively little attention. The general 
pathology of the feathered tribes is not well understood. Little 
seems to be known of their tissue reactions to injury. Their resist- 
ance to ordinary wound infections differs strikingly from that of 
mammals. Pasteur suggested that this might be due to their higher 
body temperature. On the other hand, the infectious diseases and 
parasitisms have been more carefully studied. The findings of 
many valuable researches are recorded on the nature of the more 
serious ones. Certain of them, such as bacillary white diarrhea and 



INTKODUCTION ix 

the parasitisms, have been elucidated sufficiently to enable veterin- 
arians or poultry owners to prevent them. Others that cause heavy 
losses, such as roup or diphtheria and tuberculosis, can be controlled. 
When this is done, millions of dollars worth of poultry that is now 
lost will be saved. This can be done as soon as the technical knowl- 
edge, now available, is utilized to its full extent. 

It is believed that veterinarians can render a valuable service to 
this heretofore professionally neglected, yet important industry, es- 
pecially in localities conspicuous for the raising of poultry. Be- 
cause of the relatively small value of the individual, and the large 
numbers to be dealt with, methods for preventing disease must be 
applied to the flock. With the exception of the more Valuable 
birds, individual treatment may not be practicable, but the princi- 
ples of sanitation and the preventive measures are as helpful here 
as elsewhere in the raising of animals. Veterinarians should re- 
alize that the treatment, prevention or control of diseases in poultry, 
as well as in quadrupeds, is primarily an economic question and that 
a score of dollars saved by preventing or treating diseases in fowls 
is just as essential as the saving of a like amount in sheep or calves. 
This book, dealing with the diseases and the parasites of poultry, 
will be of much aid to veterinarians who wish to render full service 
to their communities. 

V. A. Moore. 



TABLE OF CONTENTS 

CHAPTER I PAGE 

Anatomy of Birds 1 

CHAPTER II 
Hygiene and Sanitation 20 

CHAPTER III 
Apoplectiform Septicemia and Sleeping Disease 28 

CHAPTER IV 
EowL Cholera 34 

CHAPTER V 
Fowl Typhoid and Similar Infections 50 

CHAPTER VI 
Bacillary White Durrhea 68 

CHAPTER VII 
Fowl Plague 81 

CHAPTER VIII 
Avian Tuberculosis 88 

CHAPTER IX 
Avian Diphtheria and Bird Pox 96 

CHAPTER X 
Aspergillosis and Favus Ill 

CHAPTER XI 
Infectious Entero-Hepatitis of Turkeys 120 

CHAPTER XII 
Coccidiosis 127 

CHAPTER XIII 

Spirochetosis and Rare Infectious Diseases 135 

xi 



xii CONTENTS 

CHAPTER XIV PAGE 

Leukemia and Pseudo Leukemia 146 

CHAPTER XV 
General Diseases 150 

CHAPTER XVI 
Internal Parasites 178 

CHAPTER XVII 
External Parasites 208 

CHAPTER XVIII 

Infectious Diseases and Parasites of the Ostrich 226 

CHAPTER XIX 
Infectious Diseases of Geese and Ducks 242 

CHAPTER XX 
Infectious Diseases of Canary Birds 252 

CHAPTER XXI 
Tumors in Fowls 261 

CHAPTER XXII 
Toxicology 276 

CHAPTER XXIII 
Surgical Diseases 295 

CHAPTER XXIV 
Caponizing 302 

CHAPTER XXV 
Killing Poultry 314 



DISEASES OF DOMESTICATED BIRDS 



CHAPTER I 

ANATOMY OF BIRDS 

The structure of birds differs in many respects from that of 
mammals and deserves a special description. The aim of the authors 
is to brino; to the attention of the veterinarian the more important 
differences which are observed in the structure of domesticated birds 
as compared with that of domesticated mammals. The subject will 
be considered under the following; sub-divisions. 1. Skeleton, 2. 
Musculature, 3. Circulatory system, 4. ISTervous system, 5. Ali- 
mentary system, 6. Respiratory system, 7. Urinary system, 8. 
Generative system, and 0, The skin and its appendages. 

SKELETON 

Skull. The bones of the skull become united shortly after hatch- 
ing and lose their individual identity except in the case of the as- 
cending processes of the premaxillary and nasal bones which are 
not rigidly joined to the frontal bone but through their cartilaginous 
attachment permit the elevation of the superior mandible. The in- 
ferior processes of the premaxillary bone, the supermaxillaries and 
the palatine bones which form the roof of the palate do not meet 
in the median line, with the result that the palate presents an 
elongated opening or cleft. 

Vertebral column. The cervical vertebrae vary in number in 
the different species. Statements of anatomists differ concerning the 
number, because of difficulties experienced in defining cervical and 
thoracic vertebra. The atlas or first cervical vertebra is ring-like in 
form and articulates with the occipital bone of the skull by means of 
a deep concavity into which the condyle of the occipital bone is re- 
ceived. This articular arrangement and that of the other cervical 
vertebras gives the head and neck great mobility. The articular sur- 
face is concave from side to side and convex in a dorso-ventral direc- 
tion on the anterior extremity of each vertebra, presenting a saddle 
shaped appearance. The posterior extremity is the reverse, that is, 
concave dorso-ventrally and convex from side to side. 

1 



DISEASES OF DOMESTICATED BIRDS 
Nasal 45S13I 



Incisive 



Quadrate /> ou . ^ 
^.Occipital /^ Pf^^'anges 

//^■■"Metacarpus 
,/\tlas ./V^ 

-Carpus 
Ulna 



Pygostyle 




Metatarsus 



Fig. 1. The skeleton of the fowl. (Bradley) 

The thoracic vertebrae are nearly al"wajs fused together by the con- 
solidation of their spinous and transverse processes. The first may 
be free and the last may be fused -with the lumbar vertebrae. 

The lumbar and sacral regions of the vertebral column show no 
special line of demarcation. The fourteen vertebrae are consoli- 
dated into one bony mass which carries ridges on its ventral surface 
representing the transverse processes of the original independent 
vertebrae. 

The coccygeal vertebrae are seven in number. The last is the 
largest, is flattened on both sides and curves in a dorsal direction 



ANATOMY OF BIRDS d 

at the end. It is known as the pygostyle. The coccygeal vertebrse 
are movable upon each other. 

Ribs. These bones articulate dorsally with the thoracic vertebrse, 
and ventrally with the sternum by means of the inferior ribs, except 
in the case of the first two which do not reach the sternum. The 
last rib is often united to the one adjoining and does not connect with 
the sternum. Some of the ribs have flat uncinate processes which 
extend from the posterior border and lie over the external face of the 
following rib near its middle. 

The sternum is highly developed in birds and forms the floor 
of the thoracic cavity and to some extent, of the abdominal cavity. 
It is concave on its dorsal or internal face and convex on its ventral 
or external face. In fowls and pigeons a deep ridge extends along 
the median line of the ventral face. This is known as the brisket or 
keel. It serves to increase the area of attachment for the powerful 
breast muscles. The sternum of the duck and goose does not present 
as large a keel as that of the fowl and pigeon, but owing to the greater 
breadth of the sternum and more solid construction the area for 
muscular attachment is as great. In the fowl two long slender 
lateral processes are formed on each side as a result of deep notches 
which extend anteriorly into the body of the sternum. The lateral 
external process is shorter than the lateral internal process and covers 
the last two ribs with a broadened terminal bony plate. The lateral 
borders of the body of the sternum support articular facets for the 
reception of the inferior ribs. The anterior border presents an 
eminence, the episternal process to which the furculum (wishbone) 
is attached by a ligament. The articular surfaces for the coracoids 
are located on each side of the episternal process on the anterior 
border. 

Tlie internal surface of the sternum exhibits several openings 
through which air is passed to the interior of the bony structure. 

Bones of the wing. These comprise the scapula, coracoid, and 
clavicle in the shoulder region ; the humerus in the arm ; the radius 
and ulna in the forearm ; two carpal bones, the radio-carpal bone and 
ulno-carpal bone; one carpo-metacarpal bone, and three digits the 
second of which has two phalanges. 

The scapula is long, narrow, thin and curved like a sabre. It 
extends caudad over the ribs to near the pelvis. Anteriorly it is 
united with the coracoid with which it forms an articular cavity for 
the reception of the head of the humerus. The coracoid also 
articulates with the sternum by its ventral extremity. It is rod 



4 DISEASES OF DOMESTICATED BIEDS 

shaped and extends in a posterior direction obliquely ventrad from 
scapular to sternum. The coracoid at its ventral extremity presents 
an opening for the passage of air to the internal air space. The 
clavicle is attached to the coracoid at its superior end. It extends 
ventrad and caudad and curves in to the median line at the point 
of the sternum where the two clavicles unite in a flattened plate and 
become attached to the episternal process by a ligament. The united 
clavicles form a V or U shaped bone termed the fork or furculum. 
This bone represents an elastic spring and serves to prevent the 
wings from approaching each other during contraction of the de- 
pressor muscles. 

The humerus is long in palmipeds and the gallinse, and short in 
the pigeon. It is stout, slightly curved and presents a pneumatic 
foramen near its articular head. 

The ulna is much larger than the radius and is separated from it 
except at the extremities, where the two are united by ligamentous 
bands. The olecranon process of the ulna is only slightly developed. 

The two carpal bones represent fusions in embryonic life, of the 
four bones of the proximal row. The distal carpal row of three 
bones fuse with the metacarpal bones. 

Bones of the leg. These are the pelvic or hip bone; the femur 
or thigh bone; the patella, tibio-tarsus and fibula in the lower leg 
region ; a tarso-metatarsal bone, and four digits. 

The pelvic bone is made up of three bones as in mammals, the 
ilium, ischium and pubis. It differs from the mammalian bone in 
that the pelvic girdle is not complete on the ventral floor, the two 
pubic bones failing to meet in the center to form the pubic sym- 
physis. This arrangement facilitates the passing of the egg through 
the cavity. The ilium is the largest segment and extends along the 
vertebral column in the lumbar and sacral regions. It is consoli- 
dated with the last two thoracic vertebrae and the lumbar and sacral 
vertebrse, this extensive fusion giving the pelvis a rigidity which 
compensates for the lack of a pubic union. The ischium partly 
forms the side of the pelvic cavity. The pubis is mainly attached 
to the ischium along the lower border and bends inward to form the 
incomplete floor of the pelvic cavity. The ilium, ischium and pubis 
are united at the acetabulum or articular cavity for the reception 
of the head of the femur. 

The femur articulates at its distal extremity with the patella, tibia 
and fibula. The latter bone is united to the tibia, but does not ex- 
tend to its distal articulation. The tibia is comparatively long. 



ANATOMY OF BIKDS 5 

It has two articular surfaces on its distal extremity which articulate 
with the tarso-metatarsal bone. The tarsus is absent in birds. In 
males the tarso-metatarsus exhibits a slightly curved conical projec- 
tion near the distal third for the support of the spur. 

Four digits articulate with the distal extremity of the tarso-meta- 
tarsus. Three are directed radially cephalad. The internal digit 
has three phalanges; the middle, four and the external, five. The 
fourth digit is directed caudad and has two phalanges succeeding 
a rudimentary first metatarsal bone attached to the metatarsus by 
fibro-cartilaginous tissue. The distal bone of each digit is covered 
by a horny claw. 

MUSCULAR SYSTEM 

In general the muscles of birds correspond to those of mammals, 
with such modifications as are most suited to the mechanism of avian 
structure. The tendency, especially in turkeys and fowls, is to- 
ward extensive ossification of the muscle tendons. This is partic- 
ularly noticeable in the tendons of the legs but may also be observed 
in the wing and neck in some cases. The fowl and turkey also 
present a marked contrast in the appearance of the muscles of the 
breast and wings as compared with those of the legs. The breast 
and wing muscles are white, due to the relatively small amount of 
sarcoplasm in the muscle fibers. The red muscles are rich' in sarco- 
plasm. White muscles are more powerful but have less endurance 
than red ones. Free flying birds have red pectoral or breast muscles. 

The pectoral muscles are two in number, the superficial or great 
and the deep or small pectoral. The former depresses the wing 
and the latter elevates it. These muscles are very massive. The 
great pectoral muscle is attached to the clavicle, to the sternal crest 
near its border, to the posterior lateral process of the sternum and to 
the last ribs. It is inserted into the lateral tuberosity near the head 
of the humerus. It is this muscle that propels the bird in flight. 

The small pectoral muscle originates from the portion of the 
ventral face of the sternum not occupied by the great pectoral and 
also from the clavicle and membrane between the latter and the 
sternum. Its tendon is inserted into the humerus opposite that of 
the great pectoral muscle after passing through the foramen trios^ 
seum which acts as a pulley. This foramen is formed by the union 
of the scapula, coracoid and furculum. 

The diaphragm does not exhibit the muscular development of that 



6 DISEASES OF DOMESTICATED BIEDS 

of mammals. It is principally membranous with fine muscular 
bundles attached to the ribs. Two thin, delicate membranes com- 
pose the diaphragm and divide it into two planes, a pulmonary and 
a thoracic-abdominal plane. The former is spread over the in- 
ferior face of the lungs and is attached to the ribs on its border. It 
assists in respiration. The thoracic-abdominal plane has its origin 
on the dorsal spine in common with the pulmonary plane. It is 
convex anteriorly and extends to the sternum, dividing the body 
cavity into a thoracic and an abdominal cavity. It also assists in 
respiration and is particularly concerned with the abdominal air 
sacs. 

The pectineus muscle assists in the mechanical flexion of the toes 
in the act of perching on the roost. It originates on a tuberosity 
of the hip bone in front of the acetabulum and is continued by a 
long thin tendon to a short distance distad from the head of the 
tibia where it joins the flexor perforatus of the three anterior digits. 

CIRCULATORY SYSTEM 

The heart of birds is cone shaped, short and wide in the ostrich, 
elongated and possessing a more acute apex in the common fowl. It 
is placed in the anterior extremity of the thoracic cavity. Three 
veins, two anterior venae cavse and one posterior vena cava, terminate 
in the sinus of the right auricle. A peculiarity of the heart of 
birds is the absence of a tricuspid valve at the right auriculo-ven- 
tricular opening. Instead, a strong muscular fold which becomes 
closely applied to the ventricular septum during systole prevents re- 
gurgitation of blood into the auricular cavity. Two pulmonary veins 
empty into the left auricle. The left auriculo-ventricular opening 
is provided with a bi-cuspid or mitral valve. The pulmonary artery 
and aorta each has a semilunar valve. 

Arteries. The aorta gives off two innominate arteries, right and 
left brachio-cephalic, on leaving the heart and then passes over the 
right bronchus to become the descending or dorsal aorta. It con- 
tinues along the spine, giving off numerous branches, to the coccygeal 
region where it separates into three terminal arteries. 

The two carotids leave the innominate arteries and curve toward 
the ventral median line of the neck where they ascend in close prox- 
imity to each other to near the head. At the angle of the jaw each 
carotid divides into the external and internal carotid arteries. The 
arteries, especially those of the head and viscera, are distinguished 



ANATOMY OF BIRDS 7 

by their frequent anastomoses. This is also true of the veins of 
birds. 

Veins. The blood is returned to the heart by three trunks, the 
two anterior vense cavse and the posterior vena cava. The right 
jugular exceeds the left in size. The two communicate with each 
other by means of a cross branch at the base of the cranium. 

Lymphatics. The lymphatics of birds do not form two strata, 
a superficial and a deep seated, as in mammals. The latter only is 
observed. Lymphatic glands are few. The most conspicuous are 
located at the base of the neck and in the anterior thoracic cavity. 
They are replaced by plexuses of IjTiiphatic vessels surrounding the 
principal blood vessels. From the aortic plexus arise tw^o thoracic 
duets which pass cephalad on the ventral surface of the lungs and 
terminate respectively in the jugular vein of the same side. 

NOEMAL AVIAN BLOOD 

In birds as in mammals the blood is composed of a straw colored 
fluid or plasma in which float several types of blood corpuscles. One 
important difference between avian and mammalian blood, excepting 
the camel, is the presence of nuclei in the red corpuscles of the 
former. The formed elements or corpuscles are divided into two 
main divisions, the red cells or erythrocytes and the white cells 
or leucocytes. These elements vary greatly in number in different 
birds, and even in the same bird at different ages. Each cubic 
millimeter of an adult fowl's blood contains approximately 3,250,000 
red cells and 26,000 white cells, giving a percentage relation of 125 
to 1. In certain pathologic conditions this relation is markedly 
changed, the red cells rapidly decreasing and the white cells increas- 
ing in numbers. 

Red blood corpuscles or erythrocytes are straw colored, nucle- 
ated, oval, flattened discs, about 12 microns in length and 7.3 mi- 
crons in width. The nuclei take a deep blue stain with methylene 
blue, or Giemsa. The surrounding protoplasm takes a light yellow 
with methylene blue and a pink color with Giemsa's stain. 

White blood corpuscles or leucocytes are nucleated, colorless 
cells, rounded or irregular in form. They exhibit ameboid 
movement in the blood stream, some being more actively motile than 
others. The variations in their size, character of the nuclei, pres- 
ence of granules and character of the inclosed granules dift'erentiate 
these cells into five varieties. These varieties with their percentage 
ratio are as follows : 



8 DISEASES OF DOMESTICATED BIEDS 

Small mononuclear leucocytes (lyraphocytes) 40 

Large mononuclear leucocytes 18 

Polymorphonuclear leucocytes 35 

Eosinophiles 4 

Mast cells 3 

Lymphocytes. In these blood cells the nucleus is rounded or 
oval and almost completely fills the cell. It stains a deep blue with 
Giemsa. The narrow band of cell body stains a lighter blue and is 
not readily differentiated from the nucleus by ordinary staining. 
The lymphocytes are from 5 to 7 microns in diameter. 

Large mononuclears have a round or oval nucleus surrounded 
by a well defined border of cell protoplasm. The nucleus takes a 
deep blue stain, the cell body a pale blue. The cell diameter is 
10 to 15 microns. 

Polymorphonuclears have the appearance of having several nu- 
clei held together by threads or nuclear bands. They contain con- 
siderable protoplasm inclosing rod shaped or rounded granules. The 
nucleus stains blue, the protoplasm, a lighter color and the granules 
violet or brownish red with Giemsa's stain. Diameter, 10 to 15 
microns. 

Eosinophiles have an irregular nucleus. The cell protoplasm 
is filled with rounded granules which stain a bright red with Giemsa's 
stain. The nucleus takes a blue stain and the cell body a pale blue. 
Diameter, 12 microns. 

Mast cells have a lobulated nucleus which stains a deep blue. 
The cell protoplasm takes a pale stain. The granules are small and 
rounded and stain a dull violet with Giemsa and a deep blue with 
methylene blue. Diameter, 8 to 10 microns. 

Other blood cells of less importance which may be observed are 
as follows : 

Blood platelets are small colorless discs with granular centers. 
They are 3 to 4 microns in diameter and are usually found in small 
heaps of 6 to 8 cells. 

Shadow cells contain a rounded or broad oval nucleus which 
takes a deep blue stain. The cell body is colorless and not well de- 
fined or irregular in outline. These apparently represent red blood 
corpuscles undergoing degeneration. The stroma of the corpuscle 
loses its pigment, becomes colorless and gradually disappears leaving 
the nucleus partially or wholly separated. They are especially nu- 
merous in pathologic blood. 

Microblasts and macroblasts are found in the blood of voung 



ANATOMY OF BIRDS 9 

fowls. These represent red corpuscles which are smaller and larger 
respectively than the average red corpuscle. 

Myelogenous leucocytes appear frequently in young fowls. 
They are like mast cells except that their protoplasm is vacuolated. 

NERVOUS SYSTEM 

The nervous system of birds, with few exceptions, corresponds 
with that of mammals. However, there are several modifications 
which are of considerable interest. The cerebral hemispheres of 
the brain are well developed but have a smooth surface in contrast 
to the convoluted surface observed in the cerebrum of mammals. 
The cerebellum is conspicuous by the smallness of its lateral lobes. 
The optic lobes are placed in a lateral inferior position at the 
sides of the cerebellum. The large size of the optic chiasma and 
nerves indicates the paramount importance of the visual apparatus. 
The diameter of an optic nerve is equal to that of the spinal cord in 
its dorsal region. The olfactory lobes are relatively small. The 
hippocampi are absent in the cerebrum of birds. An important fea- 
ture of the nervous system of birds is the absence of nervous tracts 
leading to the spinal cord from the cerebrum. The cerebrum does 
however exert an influence over the rest of the nervous system 
through its nervous tracts connecting it with the other divisions of 
the brain. The anatomical evidence of the absence of nervous tracts 
between the cerebral hemispheres and the spinal cord is supported 
bv the absence of any marked defects of movement succeeding the 
removal of the cerebrum. The fowl so treated, on recovery from the 
operation, is not sensitive to light or sound. It fails to pick up 
grains and must be fed. Movement is not interfered with as the 
bird constantly walks about aimlessly. Its avoidance of obstacles 
shows that it is giiided by some obscure means. Ability to perch 
and to maintain its balance is not lost. The weight of the brain of 
a medium sized fowl is ten grams. 

The spinal cord of birds extends into the coccygeal vertebrae. It 
is cylindrical throughout its length except in the sacral and cervico- 
dorsal regions where two expansions are noted. The dorsal columns 
of the cord diverge from each other in the sacrum to form the cavity 
kno^ni as the sinus rhomboidalis which represents a ventricular 
dilatation of the spinal canal. The brachial plexus is formed by the 
last cervical and first two dorsal spinal nerves in ducks and geese and 



10 DISEASES OF DOMESTICATED BIEDS 

by the last three cervical and first thoracic spinal nerves in fowls, 
turkeys and pigeons. It furnishes branches to the pectoral region 
and wing. The pelvic region and legs are supplied by the lumbo- 
sacral plexus which is formed by two lumbar and four sacral spinal 
nerves. The spinal nerves vary in number according to the number 
of vertebrse present in each species. They arise from the spinal cord 
by two roots. The anterior or ventral root is motory, the posterior 
or dorsal, sensory in function. The ganglia on the latter are propor- 
tionately large. 

ALIMENTARY SYSTEM 

The alimentary system of birds differs to a considerable degree 
from that of other animals. There is no provision for mastication 
of food in the mouth owing to the absence of teeth. The food is 
taken up by the beak and is immediately passed by the tongue into 
the pharynx. From there it enters the esophagus and is carried to 
the crop where it is stored, partially softened, and slowly passed 
on to the proventriculus or glandular stomach. The gall bladder 
is absent in the pigeon and ostrich and occasionally in the guinea 
fowl. 

Mouth. The mouth is triangular in shape in such birds as the 
chicken, turkey, pigeon and canary. In the duck, goose and ostrich 
the mouth is comparatively long, with parallel borders and rounded 
anterior extremity. The roof of the mouth or hard palate is di- 
vided in the median line from near its anterior extremity to the 
pharynx, thus allowing free communication with the nasal passages. 
The soft palate observed in mammals is absent. The pharynx is 
relatively voluminous and permits the passage of large grains, or 
food masses. On its floor is the entrance to the larynx. The esoph- 
agus lacks the well developed muscular wall of mammals but rela- 
tively has a much greater diameter. 

Crop. Gallinaceous birds possess a crop or ingluvies which rep- 
resents a dilatation of the esophagus near its entrance to the thoracic 
cavity. Its wall, like that of the esophagus, consists of an outer 
membrane, a longitudinal muscular layer, a circular muscular layer, 
and an inner mucous membrane. Passage of its contents to the first 
stomach is aided by a wide circular muscle in the subcutaneous tissue 
surrounding the crop. Palmipeds, such as ducks and geese, are not 
provided with a distinct crop. Instead, the cervical portion of the 
esophagTis may become greatly distended in such a manner as to form 
a lone; fusiform reservoir. 



Fig. 2. Diagrammatic representation of 
the principal internal organs of the 
fowl. 1, tongue; 2, pharynx; 3, up- 
per portion of esophagus; 4, crop; 5, 
lower portion of esophagus ; G, proven- 
triculus; 7, gizzard; 8, origin of duo- 
denum ; 9, first branch of duodenum ; 
10, second branch of duodenum; 11, 
origin of floating portion of small in- 29.. 
testine; 12, small intestine; 12', ter- 
minal portion of small intc'^tine; 13, 
free ends of ceca; 14, origin of ceca; 
15, rectum; 16, cloaca; 17. vent; IS. 
mesentery; 19, left lobe of liver; 20, 
right lobe of liver; 21, gall bladder; 
22, spleen; 23, pancreas; 24, lung; 
(Heart not shown but located approxi- 
mately here) ; 25, ovary; 2(), o\iduct; 
27, kidney; 28, ureter; 29, up])oi 
larynx; 30, trachea; 31, 
lower larynx or syrinx ; 
32, bronchus; 33, cleft 
palate; 34, common ori- ¥• . 
fice of eustachian tubes. 
(Redrawn from Chauveau, 
with sliglit additions) 



■/3. 




12 DISEASES OF DOMESTICATED BIEDS 

In pigeons the crop is divided into two lateral pouches. In both 
male and female, marked changes take place in the mucous mem 
brane shortly before the young are hatched. The membrane becomes 
thickened, epithelial cells are rapidly proliferated, undergo fatty 
degeneration and lead to the formation of a milky fluid which accu- 
mulates in the depressions between the ridges of the mucosa. This 
fluid is used to feed the young during the first days of life. 

A certain amount of fluid is secreted by the alveolar glands of the 
esophagus which together with the water consumed serves to soften 
grains to some extent and also to produce a slight fermentation of the 
crop contents. The crop has no secretory glands other than mucous 
glands. It is connected with the proventriculus or first stomach by 
a continuation of the esophagus which passes into the thoracic cavity 
and along the ventral face of the left lung. 

Proventriculus. The proventriculus is small and fusiform in 
shape. Its walls are thick and contain numerous secretory glands 
which pour out gastric juice. The food is not held in the proven- 
triculus to be digested but after becoming saturated with the gastric 
secretion is forced into the gizzard where it is triturated by the 
powerful muscles of this organ with the aid of pebbles picked up 
by the bird. 

Gizzard. The gizzard or ventriculus bulbosus is a dense, mus- 
cular organ, flattened on two surfaces, with rounded border. In- 
ternally it is lined by a thick, tough, corrugated membrane which 
incloses a cavity of considerable volume, in which may be found 
food in various stages of disintegration and numerous pebbles, or 
bits of stone. Secretion of gastric juice also takes place in the 
gizzard according to Jobert. However, this organ acts principally 
in a mechanical way to grind the food and serves as a substitute 
for teeth. It is more highly developed in grain eating birds than 
in those subsisting principally on fish or animal food. In strictly 
carnivorous birds such as eagles, or hawks, the dense muscular wall 
is absent, or is limited to a portion of the organ, the remainder 
consisting of a membranous cul-de-sac. When reduced to a semi- 
fluid mass the food is released into the duodenum or first portion 
of the intestine, which joins the gizzard at a point near the entrance 
of the proventriculus. 

Intestines. On leaving the gizzard the duodenum extends pos- 
teriorly, bends on itself and returns to near its origin. Between 
its two parallel branches rests the pancreas which gives off its 
secretion into the lumen of the duodenum near its termination. 



ANATOMY OF BIRDS 13 

The pancreatic juice acts on the starchy material while the secre- 
tion of the proventriculus acts on the proteins in the food. Suc- 
ceeding the duodenum are, according to some writers, the other two 
divisions of the small intestine, the jejunum and ileum. These form 
several convolutions and are continued by the rectum to the cloaca. 

At the point of juncture of the small intestine and rectum, in 
certain species of birds, are found two elongated diverticula lead- 
ing from the intestine. These are the ceca or blind pouches. In 
grown fowls and turkeys they are from 4 to 7 inches in length and 
may be distended to a diameter of ^ to % of an inch. Especial 
importance is attached to them because of the fact that they are the 
seat of marked lesions in coccidiosis of chickens, and of turkeys, and 
in infectious entero-hepatitis of turkeys. In some species of wild 
birds, the ceca may reach a length of 10 inches while in others they 
are absent or merely rudimentary. Their function is apparently the 
retention of food material which has not been absorbed in passage 
through the small intestine. 

The cloaca serves as a common cavity for the entrance of the 
intestine, ureters, oviduct in the female, and vasa deferentise in 
the male. It is divided into three parts. The rectum enters the 
first part, the ureters and genital canals open on the lateral faces of 
the second and the bursa of Fabricus, a blind sac or glandular cavity, 
opens on the dorsal wall of the third or outer division. The bursa of 
Fabricus may disappear in adults. The one oviduct in the female 
opens on the left side of the second division. The material from the 
intestine and ureters is held in the cloaca to form the character- 
istic droppings and is then passed out through the anus or vent. 

Mucosa of the alimentary canal. The alimentary canal is 
lined internally by a mucous membrane which is thick, and com- 
posed of many layers of cells in the mouth, pharynx, esophagiis 
and crop. The mucosa is thin, and composed of one layer of 
columnar epithelial cells in the proventriculus, gizzard and intestine. 
In the gizzard the membrane is covered by a homy surface layer. 
In the submucous tissue of the mouth and pharynx are found 
several pairs of glands. These, however, are not considered as 
true salivary glands but produce a mucous secretion. The esoph- 
agus exhibits numerous alveolar secretory glands in the submucous 
tissue. The glandular stomach is conspicuous for the layer of 
tubular secretory glands which are set perpendicularly to the mu- 
cous membrane and which pour their secretion of gastric juice into 
the interior of the stomach. Over the mucous membrane of the 



14 DISEASES OF DOMESTICATED BIRDS 

gizzard is a tough horn-like covering formed by the hardening of 
the products secreted by the underlying simple glands. 

The mucous membrane of the intestine presents innumerable 
cylindrical elevations known as villi. It is through these that the 
digested food is assimilated and carried by means of the chyle- 
vessels or lacteals to the portal vein and thence to the liver. !N^u- 
merous goblet cells for the secretion of mucin are present in the 
villi. 

Liver. This organ is dark brown in color and composed of a 
right and left lobe, the former being the larger. The right lobe 
has a gall bladder on its ventral surface, while the bile from the 
left lobe is poured directly into the duodenum through a separate 
bile duct, the hepatic or choledic duct, which empties a short dis- 
tance behind the two pancreatic ducts. The cystic duct opens caudad 
of the hepatic duct and drains the gall bladder. 

Pancreas. This organ is long, narrow and lobulated. In color 
it is pale red. It is highly developed in birds and occupies the 
space between the two branches of the duodenum. Two or some- 
times three ducts carry its secretion into the ascending arm of the 
duodenum near its extremity and just anterior to the hepatic duct. 

RESPIRATORY SYSTEM 

The organs of respiration in birds differ markedly from those of 
mammals. They resemble more nearly the reptilian type of 
formation. 

Air passages. The nostrils are represented by two narrow 
openings at the base of the upper mandible of the beak. The nasal 
chambers are short and narrow and are separated by a septum which 
is partly bony and partly cartilaginous. The turbinated bones of 
mammals are represented by three cartilaginous structures. The 
nasal cavities open into the mouth by a common, elongated slit in 
the median line of the hard palate. Cavities known as the sub- 
orbital or infraorbital sinuses occupy a position on either side of 
the head. They commiinicate with the nasal cavity by narrow 
passages which extend from a comparatively low level in the sinus, 
upward into the nasal cavity. The arrangement prevents natural 
drainage of the sinuses. 

Birds possess an upper and a lower larynx. The former cor- 
responds to the larynx of mammals but serves only as an opening 
for the passage of air. An epiglottis is absent but its function is 



ANATOMY OF BIEDS 15 

assumed bj two lateral lips which close the laryngeal opening dur- 
ing the passage of food through the pharynx. The inferior larynx, 
or syrinx, is the voice organ. It is located in the anterior thorax 
at the division of the trachea into two bronchi. The end of the 
trachea, in fowls, is compressed from side to side and forms the 
wall of the syrinx. In certain birds the syrinx is complicated in 
structure and may be formed of a number of tracheal rings ex- 
panded to form large bony cavities. Sound is produced by the 
vibration of membranes within the walls of the lower larynx. 

The trachea is long in birds and its cartilaginous rings are com- 
plete. In the bronchi the cartilaginous rings are incomplete, a 
portion of the wall being formed by a membrane. The bronchi 
enter the lungs at the anterior extremities, become membranous and 
give off branches to these organs and to the air cells of the thorax 
and abdomen. 

The lungs are pale or bright red in color and of a spongy tex- 
ture. They are closely applied to the dorsal surface of the thorax 
and present several deep indentations into which the ribs fit. The 
ventral surface is smooth and is covered by a fold of the diaphragm. 
Only a small portion of the thoracic cavity is occupied by the lungs. 

Air sacs. These are membranous receptacles into which the air is 
carried bv terminal branches of the bronchi. Through these branches 
the cells are in direct communication with the lungs. They also, 
with certain exceptions, communicate with canals or spaces in the 
various bones, to which they supply air. The membranous wall 
is composed of two delicate layers, an external serous and an in- 
ternal mucous layer. The latter is a continuation of the mucosa of 
the bronchi, the former is regarded as a reflection of the peritoneum 
and pleura. Nine air sacs are found in the thoracic and abdominal 
cavities. The single anterior thoracic air sac surrounds the inferior 
larynx, bronchi and large blood vessels of the region. It receives 
air from the anterior part of the lungs by two openings and com- 
municates with deep seated air cells of the neck and with the cla- 
vicle, coracoid, scapula and sternum. Two lateral thoracic sacs 
receive air from the internal edge of each lung opposite the base 
of the heart. They transmit air currents to the air cells of the 
axillary region, vertebrae, ribs and humerus. The diaphragmatic 
air cells are four in number, two anterior and two posterior. They 
are inclosed between the two diaphragmatic folds. Air is received 
from the lungs but is not communicated to bony structures from 
these. Two abdominal air sacs each receive a long voluminous bron- 



16 DISEASES OF DOMESTICATED BIEDS 

chial branch which leaves the respective lung on its posterior in- 
ferior surface. These sacs extend from the lungs to the cloaca and 
are the largest in the body. They supply the bones of the pelvic 
region and femur in those species in which these bones are aeri- 
ferous. The femur of the pigeon and the humerus of the ostrich 
have no air spaces but retain their marrow. 

UEINAEY SYSTEM 

The urinary tract is composed of two kidneys each drained by a 
ureter lying along its ventral face and proceeding caudad to empty 
into the cloaca posterior to the terminus of the rectum. The kid- 
neys are elongated, reddish brown bodies divided into three prin- 
cipal lobes. They are closely applied to cavities in the pelvis on 
each side of the spinal column. These organs are not divided into 
macroscopically visible cortical and medullary zones as in mammals 
but have a homogeneous structure. In texture they are quite soft 
and rupture easily when pressed by the finger. The ureter does 
not originate in a renal pelvis but is formed by the union of several 
uriniferous tubules along the ventral face of the kidney. Its course 
may be traced by the white color of the urates which it carries, a 
material corresponding to the urine of mammals. 

GENEKATIVE SYSTEM 

The male generative organs consist of two testicles each provided 
with a vas deferens or excretory duct. The testicles are oval shaped 
organs situated in the sub-lumbar region at the anterior extremities 
of the kidneys. They vary greatly in size at different seasons, but 
show a remarkable development during the breeding season. The 
two vasa deferentise pass along the kidneys by the side of the 
ureters, exhibiting transverse convolutions along their course. 
Each opens on a small papilla situated in the uro-genital division 
of the cloaca. The base of each papilla is surrounded by a plexus 
of blood vessels which serve the purpose of an erectile tissue during 
coitus. In the drake and gander a long single penis is developed. 

The female generative organs consist of a single ovary and an 
oviduct situated on the left side of the abdominal cavity. The 
right ovary and oviduct usually fail to develop. Occasionally a rudi- 
mentary right oviduct is present. In one actively laying hen Gal- 
lagher observed a right oviduct which was nearly as long as the 



ANATOMY OF BIEDS 17 

left oviduct and equally voluminous. Its anterior extremity ex- 
hibited an infundibular membrane in contact with the ovary. Pos- 
teriorly it opened into the cloaca opposite the left oviduct. The 
appearance of its mucous membrane suggested that it was capable of 
functionating. 

The ovary is placed in the left sub-lumbar region, opposed on its 
superior surface to the ribs. In fowls it contains from twelve to 
fifteen hundred germ cells in various stages of development from 
microscopic granules to fully formed yolks in functionating ovaries. 
The oviduct terminates in the urogenital division of the cloaca just 
anterior to the left ureter. It is divided into five regions, each of 
which has a specific function. The first region, the infundibulum, 
is a delicate membrane of a funnel-like form which receives the 
ovum. Succeeding this is the part secreting albumen followed by 
the isthmus which secretes the shell membrane. The uterus or 
fourth region forms the shell. The last region, the vagina, is short 
and is provided with a sphincter muscle at its entrance to the cloaca. 

SKIN AND ITS APPENDAGES 

The skin of birds is without sweat glands. There are some small 
glands in the exterior passage of the ear, which secrete an unctious 
fluid. There is also a protruding glandular organ located above the 
coccyx between the tail feathers and known as the uropygium or 
rump gland, an organ peculiar to birds. It is round or oval in 
form and is divided into two halves by a medial septum. The exit 
passage is through a teat-like cone which projects above the level 
of the skin. Two external orifices are observed in the gland of the 
duck. In hens the gland is about the size of a pea, in geese about 
as large as a hazel nut and in the swan about an inch and one half 
in length. Its function is to secrete an oily fluid for water-proofing 
and dressing the feathers. The secretion is taken up by the beak 
and spread over the plumage. 

The feathers are complicated modifications of epidermic struc- 
ture. Each feather is composed of a quill, a shaft and a vane. 
The quill is embedded in a feather follicle of the skin and extends 
outwardly to the point where the barbs of the vane arise. It has 
an opening at its base for the reception of the dermal papilla and 
another opening at its point of junction with the vane. The shaft 
continues the quill to the extremity of the feather. The vane con- 
sists of two rows of barbs which arise on opposite sides of the shaft. 



18 DISEASES OF DOMESTICATED BIEDS 

These barbs each carry two rows of barbules which interlock with 
those of adjoining barbs. The feather is elevated by a small muscle 
located in the skin at the root of the quill. 

The comb and wattles of fowls and the caruncle of turkeys are 
developed from the skin. 

INCUBATING PERIODS 

The length of time necessary for hatching eggs by natural incu- 
bation shows some variation. The normal period for the common 
hen is 21 days but this period may be shortened to 19 or 20 days 
by warm weather and unusually constant brooding by the hen. On 
the other hand, if the eggs have been abandoned and allowed to cool 
for a time, hatching may be delayed for several days. These varia- 
tions doubtless occur in the case of other birds. The incubation 
periods of various birds, subject to variations as explained are as 
follows. 

Table I. — Incubatixg Periods 

Hen 21 days 

Pheasant 25 days 

Duck 28 days 

Peafowl 28 days 

Guinea-fowl 25 days 

Goose 30 days 

Turkey 28 days 

Pigeon 18 days 

PULSE, TEMPERATURE AND RESPIRATION" 

Loer has made an extensive series of observations on the tempera- 
ture, frequency of pulse and respiration in domestic birds. His re- 
sults are summarized as follows. 

Frequency of heart beat as determined by digital palpation after 
opening the thoracic cavity was 128 to 140 per minute in the hen 
and 141 to 149 per minute in the pigeon. The heart beat of the 
duck as determined by auscultation varied from 150 to 180 per 
minute. 



ANATOMY OF BIKDS 



19 



Table II. — Eespiration Frequency and Normal Temperatures of 

Birds 



Species 


Respiration 
frequency 


Centigrade 
degrees 


Fahrenheit 
degrees 




Min. 


Max. 


Min. 


Max. 


Min. 


Max. 


Hen 

Turkey 

Pheasant 

Pigeon 

Duck 

Goose 


12 
12 

16 
16 
12 


28 
16 

36 

28 
20 


40.5 
40.0 
41.0 
41.0 
41.0 
40.0 


42.0 
41.5 
44.0 
43.0 
43.0 
41.0 


104.9 
104.0 
105.8 
105.8 
105.8 
104.0 


107.6 
106.7 
111.2 
109.4 
109.4 
105.8 











REFERENCES 

1. Boyce and "Warrington. Observations on the anatomy, physiology and 
degenerations of the nervous system of the bird. Tr. Boy. Soc, Vol. 191, 
1899. 

2. Bradley. The structure of the fowl. London : A. & C. Black, Ltd., 
1915. 

3. Burnett. Clinical pathology of the blood of domesticated animals. 
New York: The Macmillan Cbmpany, 1918. 

4. Chauveau. Comparative anatomy of the domesticated animals. New 
York: D. Appleton and Company, 1905. 

5. Ellenberger. Handbuch der vergleichenden mikroskopischen Anat- 
omic der Haustiere. Erster Band. Berlin : Paul Parey, 1906. 

6. Ellenberger u. Baum. Handbuch der vergleichenden Anatomic der 
Haiistiere. Berlin: August Hirschwald, 1900. 

7. Kaupp. The anatomy of the domestic fowl. Philadelphia : W. B. 
Saunders Co. 

8. Loer. Vergleichend physiologische Untersuchungen liber die normal 
Rektal temperature, Atem und Pulzfrequenz der Vogel. Inaug. Diss. 
Bern, 1909. 

9. Owen. Comparative anatomy and physiology of vertebrates. Birds 
and mammals, Vol. H. London: Longmans Green & Co., 1866. 

10. Steen. Blutuntersuchungen bei gesunden Hiihnern. Inaug. Diss. 
Leipzig, 1913. 



CHAPTER II 

HYGIENE AND SANITATION 
SECURING HEALTHY STOCK 

In establishing a flock of poultry it is highly important that pre- 
cautions be taken to prevent the introduction of disease with the 
original stock. It is a common desire among beginners, to con- 
sider purchasing adult birds, in order to secure speedy returns. It 
should be borne in mind that the number of instances in which 
healthy young pullets may be purchased is comparatively rare. Too 
often hens are sold because they are old and past the best laying 
period, or because the flock has become unprofitable because of some 
disease. Fowl cholera, avian tuberculosis and diphtheria are com- 
monly introduced by the purchase of adult stock. 

Starting a flock from hatching eggs or day old chickens is the 
least dangerous method of introducing stock but there remains the 
danger of introducing white diarrhea. 

RELATION OF SOIL TO HEALTH 

"Well drained soil is desirable in that the presence of moisture 
and mud is minimized. A wet soil favors parasites. Least desir- 
able for poultry yards is sticky clay or adobe. In wet weather the 
latter soil collects on the toes of chickens in the form of balls so 
large as to impede walking. Chickens kept on such soil require 
individual treatment to free the toes, and in doing this they are 
liable to be injured. 

The continued use of a given area of soil for poultry, results 
in its becoming excessively infested with the eggs of various para- 
sites and consequently a source of danger to the birds kept thereon. 
Therefore, it is highly desirable that chickens be not kept on the 
same soil year after year. 

The problem of securing fresh areas for chickens is solved in 
various ways. Where the chicken house is a permanent, immov- 
able structure, yards may be fenced off on either side and used in 
alternate years. When birds are kept under the colony system, the 
structures necessary for the fowls are built on skids. A team may 

20 



HYGIENE AND SANITATION 21 

be hitched to the building to move it as desired. A very desirable 
method of securing fresh soil is to move chicken houses in harmony 
with a crop rotation system. In this manner a given area is cropped 
for three or four years after chickens have occupied it, before the 
land is used for birds again. When quarters are so cramped that 
no change can be made in the chicken yards, deep plowing is of 
some advantage in turning up fresh earth and covering contaminated 
soil. Small areas may be sprinkled with lime, or be thoroughly 
soaked to some depth by the liberal application of a disinfectant. 

LOCATION AND CONSTRUCTION OF POULTRY HOUSES 

Dampness is very injurious to fowls, and consequently the build- 
ings should be located with reference to securing good drainage after 
rains. Where choice is possible, sandy soil should be chosen on 
account of its permeability to water. Provision should be made to 
secure free ventilation without drafts of air. 'No especial effort 
need be made to secure warmth in a poultry house in the daytime 
even in a severe climate. The building should be so located as to 
permit the unobstructed illumination of the interior by sunlight. 

The frequency with which poultry houses must be cleaned and 
sprayed with parasiticides should be borne in mind when they are 
being constructed. Any structural detail which interferes with the 
free access to any part of a house by a man, should be avoided for 
it will interfere with routine cleaning. The habit displayed by 
mites, of collecting in cracks, should be recognized in providing 
buildings with a minimum of such places where vermin may col- 
lect. ]^est boxes, perches and similar fittings should not be per- 
manently attached to the building, but should be readily removable 
for cleaning and spraying. 

Certain details of construction will at least constitute impedi- 
ments to the dissemination of parasites and infective material from 
bird to bird. Thus, stretching chicken wire under the roosts will 
largely prevent birds from coming in contact with droppings in the 
roosting quarters. 

In houses designed for laying hens in a cold climate, each bird 
should be provided with from three to four square feet. Exercise, 
which is absokitely essential to health, will be provided by mixing 
some of the feed with clean litter on the floor. 



22 DISEASES OF DOMESTICATED BIEDS 



CLEANING AND DISINFECTING BUILDINGS 

Previous to applying a disinfectant to a building it is essential 
that all dirt and filth be removed by sweeping, scraping or washing. 
This is necessary in order to expose the woodwork to the unob- 
structed action of the disinfectant. 

A considerable range of choice of disinfectants is possible. Selec- 
tion of a disinfectant will be made on the basis of relative cheap- 
ness, availability and suitability to the requirements imposed by the 
article to be disinfected. 

Compound solution of cresol. This substance also kno^vn as 
liquor cresolis compositus, consists of a mixture of equal parts of 
cresol with a linseed oil-potash soap. It mixes well with soft water, 
but is less satisfactory in this respect when hard water is used. This 
disinfectant may be obtained at any drug store and on account of 
cheaper price is to be preferred to carbolic acid. It is employed 
for general disinfection in the proportion of four ounces to a gal- 
lon of water. 

Formaldehyde gas. Formaldehyde is ordinarily obtainable in 
a forty per cent solution in water, a product which is known as 
formalin. Formaldehyde is a strong non-poisonous disinfectant, is 
not hindered in its action by albuminous material and in general 
is not harmful to metals. The gas is a good surface disinfectant 
and may be employed in disinfecting incubators and such rooms 
as may be easily made air tight. Ordinary poultry houses are not 
constructed tightly enough to warrant the trouble of sealing all cracks. 
Under conditions warranting its use, the room in which the gas is 
to be used is carefully examined and all cracks are sealed with strips 
of paper applied with paste. 

The gas is liberated from the watery solution by mixing formalin 
with needle crystals of potassium permanganate. For each 1,000 
cubic feet of air space there should be used 20 ounces of formalin 
and 16% ounces of potassium permanganate. The permanganate is 
placed in a shallow pan with flaring sides and the proper amount of 
formalin is poured in the pan. Provision should be made to protect 
the floor as the ingredients of the mixture may splash during the 
violent reaction that ensues. Splashing will be minimized by using 
a bucket, but in this case considerable formaldehyde gas may con- 
dense on the walls of the vessel. After mixing the chemicals, the 
operator should leave the room promptly to avoid inhaling the irri- 
tating fumes. The room should be kept sealed for eight hours. 



HYGIENE AND SANITATION 23 

This method of fumigation is not applicable when the temperature 
falls below 05° F. for the gas condenses under such conditions. 

Disinfection may be accomplished by spraying objects with a 
mixture of 5 parts of formalin to 95 parts of water. 

Carbolic acid or phenol. Pure carbolic acid exists at ordinary 
temperatures as needle-like crystals. This substance is frequently 
used in the form of liquefied carbolic acid which consists of 9 parts 
of the crystals mixed with 1 part of water. Carbolic acid is ordi- 
narily emj^loyed as a disinfectant in a five per cent solution of the 
crystals. As the crystals dissolve slowly, solution is hastened by the 
use of hot water. The fluid may be applied liberally to surfaces as 
a spray, or fabrics and implements may be immersed in the fluid for 
an hour. Carbolic acid is somewhat expensive, and on this account 
some other cheaper agent may be employed. The substance in ques- 
tion should not be confused with " crude carbolic acid " which is 
quite diiferent in composition. 

Crude carbolic acid. Commercial crude carbolic acid is a by- 
product of the distillation of coal tar. It contains certain insoluble 
oils and a mixture of cresols and similar substances which possess 
disinfectant value. AVhen the content of these is known, an effective 
disinfectant may be made by including these substances in two per 
cent solution. The disinfectant in question should not be confused 
with true carbolic acid (phenol). 

Chloride of lime. Chloride of lime or chlorinated lime consists 
of slaked lime which has been exposed to the action of chlorine. 
It is a white powder which deteriorates in strength rapidly after 
opening the hermetically sealed container in which it is supplied. 
This disinfectant is particularly useful where the action of a de- 
odorant is desired besides a disinfectant. It is commonly employed 
diluted with water in the proportion of six ounces to a gallon of 
water. The presence of organic matter interferes with the effective- 
ness of this agent. 

Various coal-tar creosote disinfectants. Mixtures of various 
coal-tar products, principally creosote oil, with soap in the form of 
emulsions are on the market under a large variety of trade names. 
The disinfecting value of these products varies greatly, but when 
the carbolic acid coefiicient is stated, one of these products may be 
used with assurance as to its efficiency. The expression carbolic acid 
coefiicient, refers to the relative germicidal value of a product as 
compared with carbolic acid. 

Bichloride of mercury or corrosive sublimate. This agent is 



2-1: DISEASES OF DOMESTICATED BIRDS 

usually employed in the strength of 1 part to 1000 parts of water. 
It is available in the form of tablets mixed with ammonium chloride 
to facilitate solution in water. A tablet may be added to a certain 
specified amount of water to make a disinfectant of a definite 
strene:th. Bichloride of mercury has the disadvantage of attacking 
metals and its activity is seriously impaired by contact with albu- 
minoid substances. Its poisonous nature is some disadvantage. 

Whitewash. Whitewash is made by adding about one pint of 
water to each two pounds of freshly burned lime. The vessel con- 
taining the mixture is covered and allowed to stand for about an hour 
while slaking occurs. Water is then added to the mixture until it 
is thinned to such a consistency that it may be readily applied. 

Weather proof whitewash may be made as follows: Slake one 
bushel of quicklime in twelve gallons of hot water. Dissolve two 
pounds of common salt and one pound of zinc sulphate in two gal- 
lons of boiling water. Pour this mixture into the slaked lime and 
add two gallons of skim milk, mixing thoroughly. 

Whitewash has feeble disinfectant powers, but is useful in im- 
proving the illumination of interiors. To a certain extent it covers 
up infective material and fills up the smaller cracks which might 
harbor parasites. 

The value of scattering air slaked lime about poultry houses is 
questioned in view of the irritation of the eyes and air passages 
induced by the dust. 

Application of disinfectants. The frequency with which poul- 
try houses are disinfected warrants investment in some form of 
pump. For the smaller establishments, a pump built to be used 
in a pail may suffice. In larger poultry farms a pressure spray 
pump mounted in a barrel on wheels forms a very convenient outfit. 

CLEANLINESS OF FOOD AND DRINKING WATER 

Feeding troughs may be provided with a cover of slats in the 
form of a peaked roof. Birds will be compelled to reach through 
the slats to eat mash, and cannot walk in the feed. Sanitary water 
fountains entirely prevent birds from walking in the drinking water. 
Further protection of the drinking water by the use of potassium 
permanganate is very generally practiced. A saturated solution of 
this substance is prepared in a large bottle or jar and is kept con- 
veniently near the drinking fountain. When water is drawn for the 
birds, enough of the stock solution is added to impart a deep wine 
color to the water. 



HYGIENE AND SANITATION 25 



POST-MORTEM EXAMINATION 

The first step in making an autopsy on a bird is to examine 
carefully the exterior of the carcass for lesions of the diseases 
which exhibit external manifestations. The skin may show the 
presence of lice, mites or epithelial tumors. The head may be the 
seat of bird pox nodules, favus, or swelling due to roup. The skin 
of the head may present a pale appearance as in infectious leu- 
kemia, fowl typhoid, coccidiosis and tuberculosis or a congested or 
darkened appearance as in cholera, enteritis, pneumonia and in- 
fectious entero-hepatitis. Exudates of diphtheria may be observed 
in the mouth. Swellings of the joints of the wing or legs may in- 
dicate tuberculosis or gout. Evidence of diarrhea should be looked 
for on the feathers surrounding the vent. The general condition 
of nourishment of the bird is determined by palpation, especially in 
the breast region. 

In preparation for the examination of the internal organs it is 
best to pluck the feathers from the under surface of the body from 
the base of the neck to the vent and well up on each side of the body 
beneath the wings. The carcass is then stretched back downward 
over a table or board and held in position by cords attached to each 
leg and to the neck near the head. The other ends of the three 
cords are tied at the sides and one end of the table or board. An- 
other method of holding the carcass in position is to nail each 
foot and the neck to the board. Those who have occasion to make 
frequent autopsies find it convenient to lay the bird out on a shal- 
low, rectangTilar, flat bottomed tin pan fitted with eyelets on the 
sides and ends for the reception of cords tied to the feet and neck 
of the carcass. The pan serves to retain fluids, intestinal contents, 
etc., which may escape during the autopsy, and also is easily cleaned 
and disinfected. 

The internal organs are exposed by making an incision through 
the skin and body wall on either side of the breast near the base 
of the wing and continuing it along the side to the vent and then 
forward to a point opposite the beginning of the incision. The 
ribs may be cut through with a knife at the cartilaginous articula- 
tion between the superior and inferior ribs or they may be severed 
by means of a pair of scissors or bone forceps. The breast bone 
and abdominal wall can be removed by cutting through the b(mes 
of the shoulder girdle at the entrance to the chest with bone forceps. 



26 DISEASES OF DOMESTICATED BIEDS 

Peritoneal and other attachments are cleared away with the knife 
as the inferior body wall is being removed. 

Before removing any of the organs a general survey of the parts 
may reveal one of the following conditions : The presence of fluid 
in the abdominal cavity, which would be suggestive of peritonitis 
or enteritis; the presence of blood clots in either cavity indicating 
internal hemorrhage; yolk concretions or other egg material free in 
the abdominal cavity of females ; tubercular masses on the intestine, 
liver or spleen ; tumors in the various organs ; or moldy growths 
in the air sacs, indicating aspergillosis. 

The liver is then examined. It may be congested or show small 
necrotic spots in cholera and several bacillarv septicemias or be 
pale and enlarged in infectious leukemia and fowl typhoid. In 
tuberculosis fat-like nodules with yellowish centers would be found. 
In entero-hepatitis the areas of necrosis would be yellowish or 
greenish. Various sorts of tumors may be present on the surface of 
the liver. 

The alimentary tract requires a careful examination since many 
of the diseases are manifested by lesions at some point along its 
course. Frequently the congested areas of the mucosa may be de- 
tected through the serous membrane before the intestine is opened. 
It is advisable, however, to lay the whole tract open from the crop 
to the vent. The crop and proventriculus may show congested or 
inflamed areas as a result of the ingestion of strong irritants or 
poisons. The gizzard is relatively free of disease but may contain 
parasitic worms in its wall. The duodenum is often the seat of 
intense inflammation especially in the septicemic diseases such as 
cholera and fowl plagiTC. Coccidia also cause congestion of the 
duodenal mucosa. In infectious entero-hepatitis and coccidiosis the 
ceca are usually distended with necrotic material and the cecal 
walls are ulcerated or desquamated. In enteritis the inflammation 
may involve a considerable portion of the intestinal mucosa and may 
be observed in any part of the small intestine or in the ceca or 
rectum. The cloaca is to be inspected for evidence of vent gleet. 
Intestinal worms may be present in any portion of the intestinal 
tract. Unless present in comparatively large numbers they should 
not receive special consideration. Round worms may be found 
gathered into large masses which tend to obstruct the passage of the 
contents of the intestine. Wlien numerous they may also produce 
a catarrhal condition of the intestinal mucosa. Some tapeworms 



HYGIENE AND SANITATION 27 

when numerous cause nodular formations on the intestinal wall 
which resemble the lesions of intestinal tuberculosis. 

An enlarged, congested spleen may be associated with the acute 
bacterial septicemias. An enlarged, firm, mottled appearing spleen 
would suggest infectious leukemia. In the latter disease the kid- 
neys are also enlarged and of firmer consistency. Tubercular nod- 
ules may be present. 

A gangrenous or cystic ovary or an ovary exhibiting hard, angular, 
shrunken ova, in the case of the fowl, is practically diagnostic of 
B. puUorum infection. Occasionally gangrene of the ovary may be 
due to some other microorganism. In such cases peritonitis is apt 
to be present. 

The oviduct should be opened and examined for inflammatory 
changes, constrictions, tumors or the condition known as egg bound. 

JSTormally the lungs are found deflated and closely applied to the 
breast wall. In acute congestion and pneumonia the lungs are 
distended and stand out in a firm position surrounding the heart. 
The pneumonic lung is solidified and will sink in water. N^odular 
growths in the lungs may represent tuberculosis or aspergillosis. 
The former is much less frequently found involving the lungs of 
birds than the abdominal organs. Aspergillar nodules are usually 
accompanied by moldy growths on the mucosa of the bronchioles 
or air sacs. 

In young chickens the trachea and larger bronchi are slit open 
to discover the presence of the red worm, Syngamus trachealis, or 
of aspergillar growths. 

Pericarditis, thickened pericardial fluid or hemorrhagic points 
on the heart indicate a septicemia such as cholera or fowl typhoid. 
The pericardium and also the liver may be covered by a fine white 
deposit consisting of urate of soda crystals in visceral gout, or as 
a result of disturbances of metabolism due to a diseased condition. 

REFERENCES 

1. Kaupp. Poultry diseases and their treatment. Chicago : American 
Journal of Veterinary Medicine, 1919. 

2. Pearl, Surface and Curtis. Diseases of poultry. New York: The 
Macmillan Company, 1918. 

3. Salmon. Diseases of poultry. Washington: George E. Howard & 
Co. 

4. Salmon. Important poultry diseases. Revised by Gallagher and 
Foster. U. 8. Dep. Agr., Farmers Bull. 957, 1918. 



CHAPTER III 

APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE 
APOPLECTIFORM SEPTICEMIA 

Characterization. The disease is a liigUy fatal septicemic in- 
fection of chickens caused by a streptococcus. 

History. The disease was first described by JSTorgaard and 
Mohler in the United States and later was observed by Magnussen 
in Sweden. 

Etiology. The causative organism is a streptococcus, the in- 
dividual elements being .6 to .8 microns in diameter. There is 
great diversity in the length of chains. In tissues they are short 
and in cultures, long. 

The organism is Gram positive, non-motile, and no capsule for- 
mation has been observed. It is an aerobe and a facultative an- 
aerobe. Growth occurs on common solid and liquid media most 
abundantly at 37° C, and less rapidly at room temperature. 

In alkaline bouillon growth occurs within 24 hours at 37° C. 
Long chains develop which form skeins or balls of flocculent ap- 
pearance which are deposited on the sides and bottom of the tube. 
After three days the growth settles to the bottom in the form of a 
white non-viscid deposit. This upon agitation breaks up into nu- 
merous small particles. 

After a sparse seeding on agar, growth is visible after 24 hours 
in the form of small shiny, grayish colonies about 1.5 mm. in 
diameter. By transmitted light these appear to have a brown 
center surrounded by an irregular pale bluish border. The max- 
imum size is attained on the third day. In agar stab cultures, mi- 
nute spherical grayish white colonies with fimbriated borders, appear 
along the line of puncture. They do not coalesce, and very slight 
growth is observed on the surface. 

The surface colonies on agar plates are very similar to those 
developing on a sparsely seeded slant culture. The colonies in 
the depths of the medium are seen as minute pearly points of 
granular appearance. With the aid of a hand lens the outline ap- 

28 



APOPLECTIFORM SEPTICEMIA AND SLEEPING DISEASE 29 

pears ciliated. Similar but more profuse growth occurs on glycer- 
ine agar, and serum-gelatin-agar. 

In stab cultures on gelatin, growth is not observed until the 
fourth or fifth day. It consists of a finely granular line of minute 
spherical colonies, grayish white in color. The colonies have a 
fimbriated border and do not exceed a pinhead in size. The growth 
is not abundant nor characteristic and does not spread on the sur- 
face. 'No liquefaction occurs. Colonies on gelatin plates resemble 
those on agar, but are slightly more opalescent. 

Growth on blood serum appears within 24 hours in the form of 
small whitish colonies .6 to .8 mm. in diameter. Sometimes the 
color has a yellowish tint. The colonies do not coalesce. The water 
of condensation becomes turbid by reason of the presence of small 
gray clusters of the streptococci. 

Growth in milk occurs without causing visible change. In old 
cultures there is observed a solidification of the lower stratum, vis- 
ible when the tube is turned upside down. 

In litmus milk, the blue color is changed to a pale madder pink, 
indicating acid formation. No gi'owth occurs on potato. No indol 
is formed. 

Bouillon containing one per cent of glucose, lactose and saccha- 
rose, in fermentation tubes, forms a favorable medium. Growth 
is more profuse than in plain bouillon and extends into the closed 
arm. Gas is not produced in these sugars, but acid formation oc- 
curs. Similar results are obtained with galactose, maltose and the 
alcohols mannite, dulcite and sorbite. 

No hemolytic effect occurs in Conradi-Drigalski plate cultures. 
Acid formation occurs on litmus-lactose-agar plates. 

Morbid anatomy. The skin displays hemorrhagic discolora- 
tion on the breast and neck, due to diffuse hemorrhages in the sub- 
cutaneous and muscular tissues. The abdominal cavity contains 
an abundance of sero-sanguinous exudate. Similar exudate some- 
times is present in the pericardial sac. The veins of the mesentery 
are engorged. The liver is greatly enlarged, paler in color than 
normal and the entire surface is covered wath a semi-organized 
plastic exudate. The spleen may be similarly swollen. The gall 
bladder is distended with bile, while the kidneys are hyperemic 
and swollen. The intestines, especially the duodenum, are observed 
from the peritoneal surface to be congested in patches. On opening 
the intestines, the mucosa corresponding to the discolored areas 
is considerably swollen. The contents of the intestine consist of 



30 DISEASES OE DOMESTICATED BIEDS 

blood stained feces and mucus. The lungs show circumscribed areas 
of congestion. On opening the cranium a profuse subdural exudate 
is observed. The meninges are injected and the ventricles contain 
an abnormal amount of discolored serum. 

Symptoms. Information regarding symptoms is limited to ob- 
servations made on the behavior of inoculated cases only. A short 
time after inoculation, birds display evidence of depression. There 
is staggering gait with effort to balance with the aid of the wings. 
If the birds are not disturbed they will lie in one place until death 
occurs in coma. Sometimes diarrhea occurs immediately before 
death. 

Pathogenesis. Fowls are susceptible to intravenous or subcu- 
taneous inoculation and by the feeding of cultures. The mortality 
is heavy among fowls when the disease is spreading under natural 
conditions. Pigeons, rabbits and mice are susceptible. Intravenous 
inoculation of the duck may cause loss of coordination and death 
with endocarditis. Sparrows are more resistant than pigeons and 
chickens but succumb to large intramuscular and intraperitoneal 
doses. In the dog, intravenous inoculation causes rise of tempera- 
ture and lameness apparently due to a transitory arthritis. Ab- 
scesses may occur in the dog, a point of interest in that suppuration 
has not been observed in other animals. Guinea pigs, swine and 
sheep prove refractory. Cats may succumb to intraperitoneal in- 
oculation. Horses exhibit a disturbance of health following intra- 
venous inoculation. 

Immunization. It is possible to immunize a fowl by intra- 
venous inoculation of killed culture so that the bird will tolerate 
an otherwise fatal dose of virulent culture. Successive injections 
of virulent culture cause the blood serum to take on protective prop- 
erties, l^orgaard and Mohler have found this serum administered 
intravenously in a .5 c.c. dose, protective against a .1 c.c. intra- 
venous inoculation of culture. 



SLEEPING DISEASE 

Synonym. Schlafkrankheit, Schlafsucht, (German) ; maladie du 
somneil, (French). 

Characterization. The disease is a septicemic infection of 
fowls characterized by sjonptoms of sleepiness and caused by an 
encapsulated streptococcus. 

History. The disease was first described by Dammann and 



APOPLECTIFOEM SEPTICEMIA AND SLEEPING DISEASE 31 

Maneg'old in Germany and later by Greve in the same country. 

Symptoms. The symptom most frequently occurring is a more 
or less marked desire to sleep. The hen sits for hours at a time 
with closed eyes and ruffled feathers, with the head bent backward 
in the feathers of the neck. At interv^als the bird awakens and opens 
the beak wide as if panting. The conjunctiva, usually of one eye 
only, becomes reddened and markedly swollen. Secretion from the 
conjunctival sac dries on the edges of the lids. Except when the dis- 
ease has a very short duration, the comb and wattles gradually 
become pale. Commonly diarrhea exists for several days and the 
bird dies in a highly emaciated condition. Birds may die suddenly 
after showing sjTiiptoms for only a day or less. 

Morbid anatomy. The carcass exhibits the appearances com- 
mon in hemorrhagic septicemia, such as distention of the subcu- 
taneous veins with dark red blood, infiltration of portions of the 
musculature with bloody, watery fluid. There is bloody, shiny, 
viscid fluid in the abdominal cavity and the peritoneum is swollen 
and diffusely reddened. The mucosa of the proventriculus and of 
the intestine is swollen while that of the latter is diffusely red- 
dened. The liver is enlarged, brownish yellow in color and is fri- 
able in texture. It is studded irregularly with dark red hem- 
orrhages. The spleen is enlarged and the capsule is distended while 
the pulp is fragile in texture. The kidneys are swollen and dirty 
yellow in color. The lungs are congested and permeated with nu- 
merous small, dark red hemorrhages and may be edematous. Fi- 
brinous exudate may occur on the costal surfaces of the lungs. 
Punctiform hemorrhages may occur under the epicardium. The 
heart is distended with coagulated blood. The pericardium is often 
distended with pale serous fluid and a tough, fibrous layer of ex- 
udate frequently forms on the pericardium. Smears from the heart 
blood stained with carbol fuchsin are seen to contain chains of 
streptococci. The capsules are also seen distinctly enveloping single 
cocci as well as diplococci. 

Etiology, The streptococcus causing the disease is designated 
Streptococcus capsulaius gallinarum. It differs in the length of the 
chains and in the size of the elements according to the sort of animal 
in which it appears as a natural disease or into which it is inocu- 
lated. These differences occur also in artificial cultivation. In 
animal blood and in fluid media, chains of up to 30 elements are ob- 
served and in sugar bouillon as many as 100 elements may occur. 
The size of the single elements varies between .3 and .5 micron. 



32 DISEASES OF DOMESTICATED BIKDS 

The individuals in the chains occur as diplococci. ISTo motility is 
present. 

The streptococci are stained by all of the common anilin dyes 
and are Gram positive. With Kiihn's carbol methylene blue the 
capsules appear greenish in color. With a modification of Klett's 
anthrax capsule stain the cocci appear dark blue while the capsules 
are pale red or pink, with dark red undulating contours. The cap- 
sules are seen distinctly only in material from the animal body. 
The streptococci gi-own on the various culture media show them 
very poorly or not at all. 

The organism grows aerobically and anaerobically and its optimum 
growth temperature is that of the body. It thrives best on solid 
blood serum, and grows well in milk. It can also be grown on meat 
extract bouillon, gelatin, agar, agar gelatin and grows least well on po- 
tato. In order to cause rich gTowth an addition of 4 to 6 per cent 
of glycerin or one per cent of sugar is necessary. 

Acid is formed in saccharose bouillon and indol in limited amount. 
Gelatin is not liquefied. 

It is very sensitive to drying and also to heat. In bouillon cul- 
tures which have been warmed to 80° C, for five minutes it is killed. 
At 100° C. it is killed in % minute. One per cent solution of 
carbolic acid kills in 2 minutes, while a similar solution of liquor 
cresoli saponatus, lysol, and creolin renders it inactive in three 
minutes. 

Pathogenesis. The disease is transmitted to hens by inocula- 
tion of blood or pieces of organs as well as by inoculation with cul- 
ture. Infection with the latter succeeds through subcutaneous in- 
oculation or when finely dissipated bouillon culture is inhaled. In 
carcasses of birds dead after subcutaneous inoculation, evidence of 
coagulation necrosis is seen frequently, accompanied by infiltration 
of the surrounding tissues with bloody or purulent fluid. 

The time of appearance of symptoms in hens after artificial in- 
fection varies greatly. Sometimes sickness is noted after six days, 
with death occurring after seven days more. Again, it is possible 
for 30 to 70 days to elapse between the time of inoculation and death. 
The disease is transmissible by subcutaneous inoculation to pigeons, 
rabbits, white mice, gray mice, and lambs. The course of the disease 
is more acute in pigeons than in hens, but the lesions are similar. 
Dogs, ducks and guinea pigs do not succumb to artificial infec- 
tion. 

Differential diagnosis. The observation of capsules surround- 



APOPLECTIFOEM SEPTICEMIA AND SLEEPING DISEASE 33 

ing the streptococci in smears from tissues will differentiate the af- 
fection from apoplectiform septicemia, a very similar infection. 

Prevention. Measures similar to those recommended in the 
discussion of fowl cholera are indicated. 

Treatment. 'No medicinal treatment is available. 

REFERENCES 

1. Dammann n. Manegold. Die Schlafkranklieit der Hiiliner, Deutsche 
tierdrztl. Wchnschr., Bd. 13, 1905, S. 57Y. 

2. Greve. Beitrasr zur Kenntniss der Streptokokken-Krankheit (Schlaf- 
krankheit) der Hiihner. Deutsche tierdrztl. Wchnschr,, Bd. 16, 1908, S. 
213. 

3. Magnnssen. Ueber Eine fiir Europa neue Hiibnerseucbe. Centralhl. 
f. BaMeriol (Etc.), Oriq., 1, Alt., Bd. 56, 1910, S. 411. 

4. Norgaard and Moliler. Apoplectiform septicemia in chickens. TJ. S. 
Dep. Agr. Bureau. Animal Indust. Bull. 36, 1902. 



CHAPTER IV 

FOWL CHOLERA 

Synonyms. Chicken cholera, pasteiirellosis avium, cholera gal- 
linarum, hemorrhagic septicemia of fowls; Hiihnercholera, (Ger- 
man) ; cholera des ponies, (French). 

Characterization. Fowl cholera is an acute contagious septi- 
cemic disease affecting domesticated birds, which is accompanied by 
febrile temperature and causes heavy mortality. The popular desig- 
nation " cholera " is frequently used to indicate any highly destruc- 
tive disease of poultry. 

Etiology. The causative organism is a member of the septi- 
cemia hemorrhagica group and has been designated by various names, 
among them, Bacillus avisepticus, B. hipolaris septicus, B. avicida, 
B. cholerce gallvtiamm, and Pasteurella avium. A strain isolated 
by Ward possessed the following characteristics : 

"Morphology. The individual cells are short, non-motile rods, with 
rounded ends. They usually occur singly, but a few are seen in pairs. 
Spherical forms are numerous in actively growing cultures. The size 
varies from .4 to .6 micron broad and from 1 to 2 microns long. A bipolar 
arrangement of the protoplasm is demonstrated when carbol fuchsin and 
alkaline methylene blue stains are used. The bipolar staining is notice- 
able freqiTently in smear preparations from tissues. The presence of a 
capsule is suggested by an unstained area surrounding each organism when 
a background of stain is deposited upon the cover glass. The same appear- 
ance is noticeable in smear preparations from tissues. The organism re- 
tains the stain but faintly when treated after Gram's method. 

"Biologic Characters. The organism is aerobic and facultative anaero- 
bic. It grows readily at 37.5° C, and with much less rapidity at room 
temperature. 

"Agar. The colonies on one per cent agar, after forty-eight hours incii- 
bation at 37.5° C, appear as round, smooth, thin, shiny disks, with entire 
border and measuring about 2 mm. in diameter. Under a two-thirds ob- 
jective they appear coarsely granular and show concentric circular markings. 
They appear smoky brown in color by directly transmitted light, and gray 
by reflected light. Colonies beneath the surface are usually lenticular in 
shape, and the granular appearance is more marked under a two-thirds 
objective than in the surface colonies. After twenty-four hours the growth 
on the agar slant culture is flat, smooth, shining, translucent, grayish 
white by reflected light, and smoky brown by transmitted light, with un- 

34 



FOWL CHOLERA 35 

dulate border. The condensation water becomes decidedly turbid. After 
the first week of growth the liquid clears somewhat with the deposition of 
a viscous sediment. No pellicle has been observed on the condensation 
water. 

" Ulyccrine Agar. Growth upon this medium presents no features dis- 
tinguishable from that upon agar slant. 

" Gelatin. Surface colonies, after about two weeks' growth at room tem- 
perature, are round, vitreous masses, with entire border and smooth shiny- 
surface. A large proportion of the colonies are raised, forming a conical 
mass not exceeding 1 mm. in diameter. Such colonies appear highly re- 
fractive by directly transmitted light. Under a two-thirds objective the 
colonies have a finely granular appearance and show concentric circular 
markings. Sub-surface colonies are lenticular in shape and granular. 

" After three days' growth under similar conditions the growth in gelatin 
stab cultures is noticeable as a mass of closely aggregated colonies near 
the surface. After about two weeks the surface growth appears as a round, 
thin gray mass, with contoured surface and undulate border. At the same 
time the growth along the whole length of the path of the inoculating 
needle appears as a mass of closely aggregated distinct colonies. 

"Potato. Implantations on this medium have not resulted in visible 
growth. 

"Alkaline Bo}(illon. After forty-eight hours at 37.5° C. the fluid becomes 
slightly clouded and does not clear up on standing, even after four months. 
In cultures two or three days old no sediment is deposited, but in older 
cultures a viscous sediment accumulates. The reaction is alkaline to 
litmus and markedly so in old cultvires. No pellicle is formed, but occa- 
sionally a circular bluish band of growth adheres to the tube at the level 
of the surface of the fluid. 

"Sugar-free Bouillon. Growth is similar to that in alkaline bouillon. 

"Acid Bouillon. The growth is similar in appearance to that in alkaline, 
except that the turbidity is less marked and no accumulations have been 
noticed at either surface or bottom of liquid. Reaction becomes alkaline 
in old ciiltures. 

" MVl'. No change occurs in this medium during the length of time that 
it is ordinarily kept under observation. 

"Fermentation Tubes. (1) One per cent glucose bouillon: The liquid 
throughout the tube becomes uniformly slightly clouded in twenty-four 
hours at 37.5°C., and remains so. The reaction becomes acid in two days. 
No gas is formed. A slight amount of viscous sediment collects. 

" (2) One per cent lactose bouillon : The character of growth is similar 
to that in glucose. The reaction remains alkaline. 

" CS) One per cent saccharose bouillon : The growth is similar to that of 
the two preceding. The reaction becomes acid in two days, but eventually 
becomes alkaline in cultures several weeks old. 

"Dog Blood Serum. After twenty-four hours at ^7.^° C. the path of the 
needle is occupied by a smooth, shiny, raised growth of a color determined 
by that of the serum. The condensation water is markedly turbid. Six 
dnys later the growth, as well as the surface of a pellicle on the condensa- 
tion water, has a coppery lustre. 



36 DISEASES OF DOMESTICATED BIRDS 

" LofPer's Blood Serum. After twenty-four hours' growth at 37.5° C, 
the path of the needle is marked by a white, raised growth, with shiny, con- 
toured or smooth surface and undulate border. The condensation liquid 
becomes decidedly turbid. After several days the surface of the growth 
becomes dull. The liquid is then observed to contain a viscous sediment 
and to have patches of pellicle floating upon the surface. 

" Indol. A positive reaction is obtained in sugar-free bouillon cultures. 

"Animal Inoculation. Subcutaneous or intravenous injection of fowls 
with 1 c.c. of a 24-hour bouillon culture resulted in death in about fifteen 
hours. Doses as small as 0.05 c.c. killed in about three days. A young 
rabbit inoculated with 0.5 c.c. in an ear vein was found dead fourteen 
hours later. A guinea pig inoculated with 1 c.c. svibcvitem was found 
dead in fourteen hours. Another receiving 0.5 c.c. subcutem survived 
thirty-six hours. A pigeon swallowing 1 c.c. died in twenty-one hours, and 
another receiving 0.12 c.c. subcutem was found dead fourteen hours later." 

Pathogenicity. Besides common fowls, geese, ducks, turkeys, 
pheasants, pigeons and a large number of wild birds are susceptible 
to infection. Hemorrhagic septicemia in geese is discussed in Chap- 
ter XIX. 

The virulence of the fowl cholera organism varies greatly. Had- 
ley has shown that the minimum lethal dose for fowls may lie at 
any point between 10 c.c. and 0.000,000,000,000,001 c.c. of a 48 
hour bouillon culture. Hadley states that infection results from 
the inoculation into the breast muscle of less than fifty organisms 
and probably by the inoculation of no more than four. To test the 
infectiveness of the carcasses of fowls dead of the disease in a natural 
outbreak, "Ward fed such material to ten healthy cockerels. On the 
first day following the exposure by feeding, three birds were dead ; 
on the second day, three; on the third, fourth, fifth and sixth days, 
one bird each died. The incubation period may vary from eighteen 
hours to as many days. 

The blood and all discharges of a sick bird are infective. Eggs 
have been demonstrated to contain the virus. 

Infection may be induced in very small doses in a large variety 
of ways such as ingestion, subcutaneous, intravenous or intramus- 
cular injection, introduction of culture into the conjunctival sac, or 
into the scarified skin. 

Repeated passage of the virus through birds or through guinea 
pigs results in an increase of virulence of a strain. On the other 
hand diminution of virulence occurs under conditions not well un- 
derstood. Doubtless there are also variations of virulence with re- 
spect to the species attacked during various outbreaks. 



FOWL CHOLERA 37 

In the case of infection by ingestion the organisms are believed 
to penetrate the uninjured mucosa of the intestines and gain access 
to the lymph and thence to the blood. Death is undoubtedly caused 
by toxins. There is however, lack of unanimity of opinion as to 
whether the toxic effect is due to intracellular or to extracellular 
toxins. 

Prognosis. Prognosis is serious, for 90 to 95 per cent of acute 
cases succumb. 

Symptoms. In the pcracute form, the bird either drops dead 
suddenly or more often dies on the roost at night. 

In the acute form the first noticeable symptom in the fowl is 
the yellow color of the droppings. The yellow material consists 
of urates and is usually found on the feathers near the vent. Di- 
arrhea follows later. The discharge varies considerably in color 
and consistency. It may be a greenish mass of pasty consistency, a 
brownish red mucus or a viscous transparent fluid. The yellow 
color of the urates is the most constant character. 

Evidence of sickness is afforded by the unnatural attitude of the 
feathers and by disinclination of the bird to move about. During 
the later stages, no food is taken, but very sick fowls may drink 
copiously. Drowsiness is marked in the later stages. Frequently 
a mucous discharge drips from the mouth. The temperature varies 
from 109° to 112° F. 

Death usually occurs within three days from exposure to infec- 
tion but has been observed to occur within eighteen hours after in- 
gestion of material from the carcass of another bird dead of the 
disease. During an acute outbreak, sickness is seldom noticed more 
than twenty-four hours before death. 

The chronic form of the disease generally appears at the end of 
an outbreak. The birds are dull, depressed and show persistent or 
intermittent diarrhea. The mucosae are pale and emaciation is 
marked. Arthritis may develop in one or more joints, and leads to 
ankylosis. 

Morbid anatomy. A reddening of the skin of the breast and 
abdomen is frequently observed. The comb often is dark red in 
color, but may be pale. There is a general congestion of the blood 
vessels of the visceral organs. The heart, in almost every case, is 
studded with punctiform hemorrhages. Less frequently are observed 
a fibrinous or a gelatinous exudate in the pericardium. One of the 
lesions occurring most frequently consists of hemorrhages in the first 
and second duodenal flexures. They may be so deep seated as to be 



38 



DISEASES OF DOMESTICATED BIKDS 



visible from the peritoneal surface. Under sucli conditions the con- 
tents of the duodenum consist of a pasty mass permeated with blood 
clots. The contents of the intestines sometimes consist of a cream- 
colored pasty mass, or may be green or brownish-red in color. In 
many cases the liver is permeated with whitish punctiform areas of 
necrosis. The oral, nasal, and pharyngeal cavities frequently con- 
tain a viscid mucous fluid. 

The lungs may show congestion and catarrhal or hemorrhagic 
pneumonia. More rarely caseous foci are present. Sero-fibrinous 
exudate may occur in the air sacs. 

Hemorrhages are usually 
restricted to the heart and 
duodenum, and occur else- 
where in the intestines 
rarely. Still less frequent- 
ly are they observed to be 
abundant throughout the 
skeletal muscles. 

Microscopic examination 
of stained smears from 
heart blood and organs will 
reveal numerous bipolar 
staining rods. 

Differential diagnosis. 
Avian plague can be dif- 
ferentiated by the fact that 
no organisms are present in 
the blood as demonstrated 
by cultures or by the mi- 
croscopic examination of 
smears. Further, inoculation of pigeons and rabbits with ma- 
terial from a case of plague will not produce infection in these ani- 
mals. 

Fowl cholera has features in common with fowl typhoid. How- 
ever, diarrhea is not usual in the latter and at autopsy the intes- 
tines are found to be pale, and the contents are normal in con- 
sistency. In fowl typhoid the heart is pale and dotted with grayish 
points due to cell infiltration. A bacteriological examination is 
necessary for differentiating the various cholera-like septicemias. 
This is not necessary in practice for no information is available to 




Fig. 3. Blood smear from blood of a pigeon 
infected with fowl cholern. a, red blood 
cells; b, fowl cholera bacteria. (Klee) 



FOWL CHOLEKA 39 

warrant handling such outbreaks bj methods other than those used 
to combat cholera unless biologic products are used. 

Treatment. The treatment of individual sick birds is not rec- 
ommended, and their immediate slaughter is advised. 

Immunization. Pasteur in his memorable studies on immuni- 
zation against disease first worked with the fowl cholera organism 
in an attempt to produce an immunity against the disease caused 
by this organism. He utilized in his experiments cultures of the 
fowl cholera bacterium which he believed had become attenuated 
by exposure to air for a period of several months. His favorable 
results laid the foundation for the further study of the control 
of disease by the utilization of the specific causative organism as 
an agency of prevention. Kitt, Cogny, Vages and others working 
along the lines pursued by Pasteur have failed to substantiate his 
findings. However, it is quite possible that Pasteur worked with a 
strain of the fowl cholera organism which had immunizing value. 
Such an inference may be drawn through the researches of Hadley 
who demonstrated that a particular strain of the fowl cholera or- 
ganism designated strain 52, although practically avirulent, had the 
power, when injected in the live state, of conferring immunity to 
rabbits against the subsequent injection of a highly virulent strain. 
These findings were, to a considerable degree, confirmed by Gal- 
lagher who also found that fowls acquired a marked resistance to 
comparatively large amounts of a virulent culture following the 
injection of immunizing strain 52. At the same time the latter's 
experiments with killed cultures of several strains of the fowl 
cholera organism, including strain 52, as immunizing agents gave 
negative results. In each case fowls injected Avith bouillon cul- 
tures of organisms killed by heating at 60° C. for 1 hour, by car- 
bolizing to .5 per cent or by mixing with ether in equal parts, 
failed to show resistance to a subsequent injection of .000,000,001 
c.c. of a virulent strain. 

Mack failed to produce immunity by the use of killed organisms 
against artificial infection but claims successful results in a num- 
ber of natural outbreaks. The use of an avirulent living organism 
with immunizing properties offers the most promising method of 
prevention. One c.c. of a 24 to 48 hour bouillon culture grown 
at 37° C is injected subcutaneously. The point most convenient 
for injection is the unfeathered area of the breast beneath the 
wing. 

It is possible to produce an antiserum by injecting a horse re- 



40 DISEASES OF DOMESTICATED BIKDS 

peatedly with cultures of the fowl cholera organism. The passive 
immunity induced by its injection into fowls is short, and its use- 
fulness is limited to flocks already infected or in grave danger of 
becoming so. 

Immunization with an aggressin has been accomplished in an 
experimental way by Weil. He produces a pleural exudate in a 
rabbit by injecting with fowl cholera bacilli. This exudate is car- 
bolized and heated for three hours at 44° C. A dose of 5 c.c. is said 
to immunize against subsequent injection of a lethal dose. 

Prevention. Sanitation with reference to known methods of 
dissemination should be the basis of combating the disease. The 
chief sources of infection within an infected flock are dead birds 
eaten by members of the flock, and contamination of food and water 
by droppings. On large poultry farms, measures to secure isola- 
tion of the center of infection should be enforced promptl3^ This 
may involve temporary fencing, or moving the buildings, if portable. 

Daily inspection of the roosting houses at daybreak should be 
made to remove dead birds and to secure sick ones before they have 
opportunity to go afield. Constant watch during the day will reveal 
droopy birds which should be killed. 

Feeding troughs may be so arranged that the birds can only put 
in the head and do not have opportunity to contaminate the feed 
with their feet. The drinking water may be rendered safe by 
adding to it mercuric chloride in the proportion of one part to six 
thousand parts of water. Earthenware containers should be used. 

Disinfection of houses and adjacent areas should be carried out 
daily. Since the floor of the roosting house is highly contaminated 
by droppings, it should be disinfected if possible, before the birds 
leave the roost. At any rate, the birds should be excluded from the 
roosting house until it is possible to disinfect. 

Poultrymen, familiar with the ravages of cholera, have been 
knowTi to ship sick and exposed birds to market, as the simplest 
way to avoid financial loss. Apart from the obvious effect in re- 
moving a center of infection, it has another effect in further spread- 
ing infection. Birds dying during the trip to the shipping point 
are thrown by the roadside, where they are liable to be partially 
eaten by any fowls encountering them. The disease may be intro- 
duced into a flock in a large number of ways such as introducing 
birds in the incubation period of the disease, the carrying in of 
infection on the shoes, by water, by animals, by pigeons or wild 



FOWL CHOLERA 41 

birds. All these possibilities, except perhaps the last two, suggest 
appropriate defensive measures. 

EDEMA OF THE WATTLES OF FOWLS 

Characterization. Edema of the wattles is an infectious dis- 
ease involving the w^attles and which usually runs a chronic course. 

History. The disease has been described by Seddon who ob- 
served it among fowls in the suburbs of Melbourne, Australia. 

Etiology. From all acute cases it is possible to isolate a short 
rod indistingTiishable from the one causing fowl cholera. In view 
of this fact and since fowl cholera is very common in the region 
in question it is likely that the wattle lesion merely represents a 
localized chronic form of disease caused by the fowl cholera bac- 
terium. 

Pathogenicity. Scarification of the wattle of fowls and rubbing 
in of culture in one case resulted in general illness, conjunctivitis, 
edema of wattle, diarrhea and formation of necrotic material. The 
bird when killed showed little change beyond the head lesion which 
was found to contain the organism that was inoculated. Another 
fowl inoculated in the same way showed edema and necrosis at the 
point of inoculation. The bird subsequently displayed immunity 
to infection through scarification or by subcutaneous injection of 
virulent culture. A hen receiving one fourth c.c. of culture intra- 
muscvilarly died in 24 hours and showed septicemic lesions at au- 
topsy. 

The disease occurred spontaneously among White Leghorns pos- 
sessing large wattles. These brushed on the ground during feeding, 
which offered an opportunity for injury and infection. Wounds re- 
ceived during fighting offer another opportunity for entrance of 
virus. 

The pigeon is killed by intramuscular inoculation of culture. 
Eabbits succumb to the infection with lesions of hemorrhagic sep- 
ticemia. 

Symptoms. There is sudden enlargement of the wattles due to 
more or less distention with fluid. In the beginning stage the wat- 
tles are hot, dark red in color and upon incision a clear fluid exudes. 
The birds manifest symptoms of general illness, loss of appetite, etc. 
Sometimes there is conjunctivitis. Subsequently there is gi'adual 
absorption of fluid accompanied by thickening of the wattle by 
fibrous tissue. ISTodules sometimes form in the tissues beneath the 



42 DISEASES OF DOMESTICATED BIEDS 

mandible or under the scars of wounds acquired during fighting. 
The morbid process leads to disfigurement of the wattles by swell- 
ings and bj their assmning a crinkly form. In a small percentage 
of cases of the disease fatal septicemia occurs. 

Morbid anatomy. The more highly thickened areas in the wat- 
tles consist of masses of caseous material. In some cases the ne- 
crotic mass is surrounded by fibrous tissue, yellowish brown in 
color and hard, almost horny in texture. 

Treatment. Cropping the wattles offers the most satisfactory 
means for dealing with the infection. The operation is described 
on page 298. 

Prophylaxis. Preventive measures must be essentially those 
employed against fowl cholera. 

CHOLERA-LIKE SEPTICEMIAS 

The literature contains descriptions of a considerable number 
of acute infections occurring among fowls, turkeys, geese, ducks, 
swans and other birds. In a number of instances the diseases have 
been shown not to be fowl cholera by bacteriological evidence that 
is convincing today. In other instances the features differentiat- 
ing the disease from fowl cholera do not appear convincing at the 
present time. The reports cover a considerable period of time 
during which many changes have occurred in methods of identify- 
ing cultures. Thus the old bacteriological descriptions are inade- 
quate for making an accurate classification of these infections. 

There is little practical need for a close examination of the 
etiology of these septicemias. The general methods of prophylaxis 
are identical with those necessary in combating fowl cholera. 

DISEASES IDENTICAL WITH FOWL CHOLERA 

There are examples of diseases substantially identical with fowl 
cholera which have been described under different names or without 
assignment of name. Lisi described a fatal septicemia occurring 
in fowls which caused the death of all the birds in the flocks in- 
vaded. J^ocard and Leclainche agree with Lignieres that the dis- 
ease was fowl cholera. Eabieaux observed a disease which he des- 
ignates as a hemorrhagic septicemia of the duck and fowl. Lig- 
nieres as well as Hutyra and Marek agree that Eabieaux does not 
show that the disease described by him is different from fowl cholera. 



FOWL CHOLERA 43 



EPIZOOTIC DYSENTERY OF FOWLS AND TUKKEYS 

Lucet describes a septicemic disease of fowls and turkeys. He 
differentiates the disease from fowl cholera by the insusceptibility 
of the rabbit to subcutaneous inoculation and other peculiarities even 
less convincing. 

Etiology. The organism causing the infection is a short, slightly 
motile rod which does not stain by the Gram method. It does not 
grow on potato and gelatin is not liquefied. 

Pathogenicity. The disease is inoculable from fowl to fowl, 
from the fowl to the turkey, from turkey to turkey and reciprocally. 
It is also transmissible between the two species by ingestion. The 
pigeon is insusceptible to subcutaneous inoculation. The gTiinea 
pig is not affected by subcutaneous or intraperitoneal injection. The 
rabbit is insusceptible to injections in the same way, but succumbs 
to intravenous inoculation. 

Symptoms and lesions. There is nothing distinctive in the 
symptoms displayed while the lesions are those of fowl cholera. 

EPIZOOTIC PNEUMO-PERICAKDITIS IN THE TURKEY 

Characterization. The disease is an infection of the turkey 
characterized by lesions of the lung and pericardium. 

History. M'Fadyean first described the infection in England, 
while Jowett encountered it near Cape Town. 

Etiology. The organism causing the disease is a small ovoid rod 
closely resembling that causing fowl cholera. M'Fadyean notes that 
it possesses motility, while Jowett is silent on the point. It is Gram 
negative and is readily stained by the ordinary dyes. No lique- 
faction is produced in gelatin, no gas is formed in agar shake cul- 
tures, no acid formation nor coagulation occurs in milk and no vis- 
ible growth is observed on potato. Growth occurs equally well under 
aerobic or anaerobic conditions. 'No unusual or striking character- 
istics are presented by the growth on agar slant or bouillon cultures. 

Pathogenicity. In the natural outbreak observed by Jowett, 
turkeys only succumbed, while fowls, geese and pigeons in close 
contact with them escaped infection. Subcutaneous inoculation of 
the turkey with cultures caused symptoms of dullness, stiffness and 
mouth breathing followed by death in a few days. Guinea pigs 
and rabbits succumb to inoculation. Fowls are only slightly sus- 
ceptible while pigeons succumb to intraperitoneal inoculation. 



44 DISEASES OF DOMESTICATED BIEDS 

White rats die after intraperitoneal inoculation, but subcutaneous 
inoculation may fail. 

Morbid anatomy. Severe pericarditis is one of the most no- 
ticeable characteristics observed at autopsy. The pericardium may 
show extensive adhesions to the heart wall, and the latter may be 
covered with a layer of yellow colored fibrinous exudate. The peri- 
cardial sac may contain sero-fibrinous exudate. The lungs show 
pneumonic changes and are frequently completely hepatized. Be- 
yond possible fatty changes in the liver and paleness and swelling 
of the kidneys, changes in other organs are not marked. 

Microscopic examination of blood smears from heart blood, peri- 
cardial exudate, lung and various organs, reveals the presence of a 
bipolar rod. 

Relation of disease to fowl cholera. MTadyean believes that 
the effects produced on various animals by the organism described 
by him, warrant the differentiation of the disease from fowl cholera. 
He notes that pericarditis and pneumonia occur in fowl cholera, but 
not with such constancy as they occur in the disease described by 
him. 

AN EPIZOOTIC AMONG FOWLS 

Mazza reported upon a disease that caused heavy mortality in 
various parts of upper Italy. 

Etiology. Cultures from various organs almost always yield 
growth of a motile rod, while culture media seeded from exudate, 
blood and brain are more often sterile. Mazza concludes that the 
organism differs from that of fowl cholera in several particulars. 
It is larger than B. avisepticus, does not usually exhibit bipolar 
staining, is motile, is not very pathogenic for rabbits and is rarely 
observed in the blood. 

Pathogenicity. Hens and pigeons succumb to the infection 
without exception. Guinea pigs are completely insusceptible while 
rabbits are very slightly susceptible. 

Symptoms. In general the hens die suddenly during the night 
without having previously shown distinct symptoms of disease. In 
other cases, symptoms like those occurring in fowl cholera are ob- 
served. 

Morbid anatomy. In external appearance the fowls usually 
show no signs of emaciation. The only abnormal conditions en- 
countered are darkening of the comb and large red areas on the skin 
of the abdomen and of the breast. The subcutaneous cellular tissue 



FOWL CHOLEEA 45 

appears scanty and occasionally hemorrhages are observ^ed in this 
locality. Quite constant lesions are encountered in the chest and in- 
volve one or both lungs. There is a serous exudate in the chest 
cavity sometimes with other signs of inflammation. More rarely 
there is observed serous bloody fluid in the pericardium and red- 
dening of the mucosa of the duodenum. In the cranial cavity there 
is rarely observed a reddening of the pia mater and of the brain 
substance. 



HEMOKRHAGIC SEPTICEMIA OF THE RING DOVE 

Leclainche reports the occurrence of a septicemic disease of ring 
doves from which he isolated an organism regarded as belonging 
to the hemorrhagic septicemia gi'oup. 

Etiology. The causative organism is an ovoid rod identical in 
shape with that causing fowl cholera, but somewhat larger. The 
organism shows bipolar staining and is Gram negative. Growth 
occurs on potato and gelatin is not liquefied. 

Pathogenicity. The infection is transmissible to the ring dove 
by inoculation and by ingestion. The domestic pigeon is much more 
resistant. The fowl is absolutely refractory while the rabbit and 
guinea pig are susceptible. 

Symptoms. The symptoms are those usually presented by birds 
affected with a septicemia. 

Morbid anatomy. Lesions consist chiefly of hemorrhagic in- 
flammation of the small intestine. 



CHOLERA OF COSCOROBA SWANS 

Tretrop observed a septicemia among swans in the zoological gar- 
den of Antwerp to which he has given the above designation. The 
species involved was Coscoroha Candida. About fifty birds were in 
the flock, of which the majority died. A large number of other 
species of swans and other waterfowl were in contact with the dis- 
eased ones but escaped infection. 

Etiology. There is found constantly in the organs of the dis- 
eased birds, a microorganism designated Bacillus coscoroba. It is 
an ovoid motile rod 1.5 to 2.5 microns long and 1 to 1.4 microns 
broad. Bipolar staining is observed and the organism is Gram 
negative. The organism grows equally well in bouillon, milk, gel- 



46 DISEASES OF DOMESTICATED BIRDS 

atin and not on potato. Milk is coagulated and indol formed. Gel- 
atin is not liquefied. 

Pathogenicity. The mouse is very susceptible to inoculation but 
the white mouse will not contract the infection by ingestion. Birds 
of the order passer es succumb rapidly to intramuscular injection 
of culture. The duck and fowl are insusceptible. Numerous spe- 
cies of swans, geese and ducks in contact with the diseased birds, 
escaped infection. 

Symptoms. The birds remain in a squatting position, and show 
the usual manifestations of sickness exhibited by those affected with 
a septicemia. 

Morbid anatomy. The subjects are generally in good condi- 
tion. The muscles offer nothing special and the heart appears nor- 
mal. Commonly, active congestion is observed in the lungs. Some- 
times one or two caseous foci are present, which are easily enucle- 
ated. The liver is enlarged, dark in color and frequently shows 
small whitish spots. The spleen is sometimes slightly engorged, 
sometimes slightly increased in size. The intestine always shows 
diarrhea with contents yellowish or yellowish gi-een in color. The 
intestines do not show marked injection of the blood vessels. No- 
dules the size of a small pea are frequently found in the abdominal 
cavity in the vicinity of the vertebral column. 

HEMOKRHAGIC SEPTICEMIA OF THE SWAN 

Fiorentini observed a septicemic infection among swans in the 
zoological gardens of Milan. 

Morbid anatomy. In young birds that have died quickly there 
is an edematous infiltration of the lungs with ecchymoses on the 
serous membranes. There is also a slight hyperemia of the intes- 
tinal mucosa, dark blood clots in the heart cavity and cloudy degen- 
eration of the liver cells. In older birds that have died after several 
days sickness there are more severe lesions. The lungs show fibrous 
pneumonia in the stage of gray hepatization. The upper lobes of 
the liver show a grayish yellow exudate composed mostly of lym- 
phoid elements, besides marked thickening of Glisson's capsule. 
The hepatic tissue shows a marked infiltration with red blood cells 
in the spaces between the liver cells. In numerous places in the 
liver there are yellowish zones caused by the fatty degeneration of the 
cellular elements. In the intestine there is slight hyperemia but 
no exudate nor swelling. On the serous membranes there are numer- 



FOWL CHOLEKA 47 

ous confluent ecchymoses, especially along the course of the coronary 
arteries. 

Etiology. The blood of dead swans yields cultures of a short rod 
with rounded ends and which shows bipolar staining. The shape 
of the organism is very similar to that of the fowl cholera bacterium, 
but it is somewhat larger. The organism has some characteristics 
in common with that of fowl cholera. Both stain alike by the Gram 
method and do not give an indol reaction. However, they differ 
in other characteristics as the swan organism is motile. It also 
forms rods as long as 4 microns. Growth in bouillon, agar and gel- 
atin furnishes no distinguishing characteristic. Copious brown col- 
ored growth occurs on potato accompanied by a bad odor. 

Pathogenicity. The organism is virulent for the swan and a 
goose (A'iiser aegyptiacus) while various aquatic and other birds 
escaped infection. 

Rabbits, guinea pigs, ducks, geese, hens and pigeons succumb to 
intramuscular inoculation of culture. 



INFECTIOUS ENTERITIS OF PHEASANTS 

Fiorontini observed an epizootic among pheasants in the public 
gardens of Milan which occurred a short time after an epizootic 
of the same nature among swans. The disease was slightly con- 
tagious for after many months the greater part of the birds escaped 
infection. 

Etiology. The organism causing the disease resembles that of 
fowl cholera. It measures .7 micron in diameter and 1 to 2 mi- 
crons in length. In cultures the organism forms chains which are 
sometimes very long. Growth in bouillon is rapid at 22° to 24° C. 
Indol is produced. On gelatin in 48 hours, a gray layer of gro^\i;h 
develops. On potato the color varies according to the development 
of the growth. After 48 hours, the color is pale yellow, which 
changes to brown while the borders are rose brown. The culture 
has the appearance of honey. 

Pathogenicity. Pheasants alone are attacked and a preference 
for males is exhibited. The infection is transmitted by inoculation 
of cultures subcutaneously or intravenously in small amounts. In- 
gestion of culture induces disease identical with that occurring natu- 
rally. Hens are not affected by receiving 2 to 3 c.c. of virulent 
culture and such inoculation does not assure immunity to fowl 
cholera. Eabbits and gxiinea pigs are immune. 



t' 



48 DISEASES OF DOMESTICATED BIRDS 

Symptoms. The birds display depression and the gait is uncer- 
tain. The appetite is poor. Late in the disease an abundant di- 
arrhea occurs, with the passage of gTayish yellow or greenish colored 
material. The state of coma and somnolence seen in fowl cholera 
does not occur. The attack lasts five to eight days. 

Morbid anatomy. Lesions occur throughout the intestine. The 
mucosa is congested, is reddish brown in color and is covered with 
a viscid layer or by a croupous exudate. Ecchymoses are not found 
on the serous membranes. The liver is friable and the spleen is 
swollen but not hemorrhagic. 

REFERENCES 

1. Fiorentini. Enterite infettiva del fagiani. Atti della Societa 
iialiana di scenze naturali, 1896, p. 89. 

2. Fiorentini. Hamorrhagische Septikamie der Scliwane. Centralhl. f. 
Balteriol. {Etc.), 1. Alt. Orig., Bd. 19, 1896, S. 932. 

3. Gallagher. Fowl cholera and other hemorrhagic septicemia immuni- 
zation experiments. J. Am. Vet. M. Ass., Vol. 50, (n.s. Vol. 3), 1917, 
p. 708. 

4. Hadley. Fowl cholera and methods of combating it. Rhode Island 
Agr. Exp. 8ta. Bull. lU, 1910. 

5. Hadley. A biological study of eleven pathogenic organisms from 
cholera like diseases in poultry. Rhode Island Agr. Exp. Sta. Bull. 146, 
1910. 

6. Higgins. Notes upon an epidemic of fowl cholera and upon the com- 
parative production of acid by allied bacteria. Jour. Exper. Med., Vol. 3, 
1898, p. 651. 

7. Jowett. Epizootic pneumo-pericarditis in the turkey. J. Comp. 
Path, and Therap., Vol. 21, 1908, p. 324. 

8. Kitt. Die Serumimpfung gegen Gefliigelcholera. Monatshefte f. 
praU. Tierh., Bd. 16, 1904, S. 1. 

9. Leelainche. Sur une nouvelle septicemic bemorrhagique. La maladie 
des palombes. Ann. de V Inst. Pasteur, T. 8, 1894, p. 490. 

10. Lucet. Dysenteric epizootique des poules et des dindes. Ann. de V 
Inst. Pasteur, T. 5, 1891, p. 312. 

11. Mazza. Bakteriologische Untersuchungen liber eine neuerdings auf 
getretene Hiihnerepizootie. Centralhl. f. Bdkteriol. (Etc), 1. Aht. Orig., 
Bd. 26, 1899, S. 181. 

12. Mack and Records. The use of bacterins in the control of fowl 
cholera. Univ. Agr. Exp. Sta. Bull. 85, 1916. 

13. M'Fadyean. Epizootic pneumo-pericarditis in the turkey. J. Comp. 
Path, and Therap., Vol. 6, 1893, p. 334. 

14. Nocard and Leelainche. Les maladies microhiennes des animaux. 
Paris : Masson et Cie. 1903. 

15. Pasteur. De 1' attenuation du virus du cholera des poules. Compt. 
Rend. Acad. Sci. Paris, T. 91, 1880, p. 673. 



FOWL CHOLERA 49 

16. Pasteur. Sur les maladies virulentes, et en particular sur la maladie 
appelee vulgairement cholera des poules. Compt. Rend. Acad. Sci. Paris, 
T. 90, 1880, p. 239. 

17. Rabieaux. Sur une septicemie hemorrhagique du canard et de la 
poule. J. de med. vet. et de zootech., T. 51, 1900, p. 129. 

18. Seddon. Oedema of the wattles of fowls due to an organism of the 
pasteurella group. Vet. J., Vol. 21, 1914, p. 24. 

19. Seddon. A diseases of the wattles of the fowl. J. Agr. Victoria, 
Vol. 12, 1914, p. 426. 

20. Tretrop. La maladie des cygnes coscoroba. Ann. de V Inst. Pasteur, 
T. 14, 1900, p. 224. 

21. Ward. Fowl cholera. Uiiiv. of Cat. Agr. Exp. Sta. Bull. 156, 1904. 



CHAPTER V 

FOWL TYPHOID AND SIMILAR INFECTIONS 
FOWL TYPHOID 

Synonym. Hiibner typhus (German). 

Characterization. Fowl typhoid is a specific infectious disease 
of fowls, having the general characteristics of a septicemia and is 
caused by Bacterium sanguinarium (Bacillus gallinarum). 

History. The disease seems to have been first described by Klein 
in England in 1889 under the name of infectious enteritis of fowls. 
The organism was designated by him, Bacillus gallinat^m. Had- 
ley states that a culture of this organism has been preserved since 
its isolation by Klein, and that a study recently made by him re- 
veals the organism to be identical with Bacterium sanguinarium. 
The disease and its causative agent were described by Moore in 
1895. Other outbreaks in the United States have been described by 
Dawson, Curtice and by Taylor. 

Pfeiler and Eehse observed the same disease in 1912, gave it the 
name " Hiihner typhus," and described the organism under the name 
Bacterium typhi gallinarum alcalifaciens. A second outbreak oc- 
curring in 1915 has been described by Pfeiler and Roepke, 

Etiology. The characteristics of the organism are described by 
Moore as follows: 

" Morpliology. Bacterium sanguinarium varies somewhat in size ac- 
cording to the medium in which it has developed. In tissues of fowls or 
rabbits it is from 1.2 to 1.8 microns long and from 1 to 1.3 microns broad. 
The ends are tapering or rounded in cultures ; in the short forms it could 
easily be mistaken for a micrococcus. In tissue it frequently appears in 
small clumps, but usually in pairs imited end to end. Spores or vacvioles 
have not been discovered. Involution forms are common. In cultures on 
agar it is more slender than in tissues. When examined in a hanging 
drop preparation, especially at the edge, it frequently shows a marked 
polar arrangement of the cellular protoplasm. In these preparations there 
is observed a marked dancing motion of the organism. In old bouillon 
cultures short chains composed of these organisms united end to end are 
sometimes observed. 

" Staining. It stains with the aniline dyes ordinarily used, btit retains 
the coloring matter very feebly, or not at all, when treated after the Gram 
method. 

50 



FOWL TYPHOID AND SIMILAR INFECTIONS 51 

" Cultivation. This organism is readily cultivated on the ordinary 
media. It is obtained in pure cultures from the heart blood or liver of a 
fowl just dead from the disease. 

"Agar. On this medium, at 37° C, the growth is moderately vigorous. 
It has a grayish glistening appearance. Isolated colonies are from 1 to 
2 mm. in diameter, convex, and with sharply defined borders. Agar plates 
emit a peculiar penetrating odor, which differs decidedly from the pungent 
odor given off by Bacterium suisepticum. The growth on this medium 
resembles very closely that of B. suipestifer. 

" Gelatin. In this medium the growth is less vigorous. In stick cul- 
tures it is more abundant along the line of inoculation than on the svirface. 
Isolated colonies are about 0.25 mm. in diameter, appearing to the un- 
aided eye as homogeneous bodies, but slightly granular under low mag- 
nification. On the surface of the gelatin the colonies are granular and 
slightly spreading. They are not characterized by any distinctive mark- 
ings. There is no liquefaction or softening of the medium. 

" Potato. On the surface of potatoes a delicate grayish yellow growth 
appears after forty-eight hours when kept at a temperature of 35° C. 
Frequently there is no development, owing, presumably, to the acids in the 
potato. 

" BotiUlon. In alkaline peptone bouillon at 36° O. the growth imparts 
a uniform cloudiness to the liquid within twenty-four hours. If the 
bouillon contains much sugar the reaction becomes acid, otherwise it re- 
mains alkaline. A grayish friable sediment forms in the bottom of the 
tube. After several days' standing the growth settles, leaving a clear 
supernatant fluid. In a simple peptone solution containing one-half of 1 
per cent sodium chloride the growth is less vigorous than in the one con- 
taining the meat juice. In meat extract bouillon the growth is likewise 
feeble. In acid peptone bouillon there is a very faint cloudiness imparted 
to the liquid. 

" Alkaline bouillon containing 1 per cent dextrose in the fermentation 
tube becomes cloudy within twenty-four hours afteir inoculating' and 
strongly acid in reaction. Similar tubes of bouillon containing saccharose 
and lactose become clouded throughout but they remain alkaline in reac- 
tion. The degree of alkalinity increases with age. Gas is not produced 
during the growth in bouillon containing these sugars. 

"Life condition.s and properties. This organism develops at a temnera- 
ture from 20 to 41° C. It does not grow well in acid media. It produces 
indol. 

"Resistance. It is destroyed at 50° C. in fifteen minutes. A 1 per 
cent solution of carbolic acid was fatal to it in 5 minutes. It resists 
drying when in films on cover-glasses for from 7 to 15 days. 

"Pathogenesis. This organism is fatal to fowls, pigeons, rabbits, guinea 
pigs, and mice. Other animals have not been tested. Excepting in in- 
travenous injections, comparatively large quantities of a pure culture 
were required to produce fatal results. Fowls inoculated in the wing vein 
with 0.3 c.c. of a fresh bouillon culture died in from three to thirteen 
days; usually on the fifth or sixth day. The temperature begins to rise 
on the second day after inoculation. It reaches 109 to 111° F. a few days 



52 DISEASES OF DOMESTICATED BIEDS 

before death occurs. In cases vphere the fowls live from five to six days 
they appear perfectly well for at least three days, when the feathers begin 
to have a slightly ruffled appearance. Pigeons inoculated with 0.2 c.c. of 
a bouillon culture die in from four to five days. In rabbits the lesions re- 
semble very closely those produced by attenuated hog cholera bacteria 
(B. suipestifer). Guinea pigs inoculated in the abdominal cavity with 
from 0.2 to 0.3 c.c. of a bouillon culture die in from five to eight days." 



Differences from B. puUorum. The two causative organisms 
differ materially in their action on sugar media. B. pulloimm pro- 
duces gas in dextrose, mannite and levulose, while B. sanguinarium 
does not produce gas in any of the sugars in common use. Milk is 
rendered acid by B. pullorum and alkaline by B. sanguinarium with 
or without saponification in the latter instance. B. pullorum is neg- 
ative to the methyl red test when grown in 1 per cent maltose bouil- 
lon, while B. sanguinarium gives a positive reaction. 

Symptoms. These are quite similar to those of other acute 
septicemic diseases. Drowsiness and indifference to surroundings 
are marked. There is loss of appetite and general weakness. The 
head may be drawn in close to the body or may hang limp. The 
mucosae of the head are pale. Diarrhea is present in the majority 
of cases. The droppings are yellowish and may be tinged with 
green. The comb and wattles are usually paler than normal but 
may be darkened with venous congestion. The blood is pale red 
in color and presents a marked decrease in red cells and great in- 
crease of white cells. The period of incubation is four to six days 
and the duration of symptoms in fatal cases from four to twelve 
days. A temperature elevation of three to five degrees is noted. 

Morbid anatomy. There is a general anemic appearance of the 
serous membranes. The mucous membrane of the intestine is usu- 
ally pale. At times it may show slight areas of congestion, or hem- 
orrhagic points. The most marked changes observed on post mortem 
examination are in the liver, spleen, kidneys and blood. The liver 
is greatly enlarged and generally dotted with grayish necrotic spots. 
It may, at times, be congested throughout or show spots or bands of 
congestion. It has a tendency to become friable. Microscopic ex- 
amination of sections of the organ reveals an engorgement of the 
blood vessels and a breaking down of the parenchymatous tissue. 
The hepatic cells present different stages of degeneration from cloudy 
swelling to complete necrosis. The necrotic areas vary in size from 
that of a few cells to macroscopic lesions. The spleen is sometimes 



FOWL TYPHOID AND SIMILAR INFECTIONS 



53 



enlarged, dark colored and pulpy. It may show necrotic points. 
The kidneys are somewhat enlarged, may be lighter in color and 
slightly injected with blood. 

The vascular system shows the most constant changes. The heart 
appears normal or else pale with grayish spots of necrosis. The 
blood is lighter in color and does not clot readily. Microscopic ex- 
amination reveals a great disproportion between the number of red 
and white cells present. The red cells decrease in numbers to a 
marked degree as the disease advances while the white cells become 
greatly increased in numbers. This increase is confined principally 
to the polymorphonuclear leucocytes. The following table from 
Moore will illustrate the proportionate relationship between the red 
and white cells during the course of the disease. 



Table III. — Blood Changes in Fowl Fed Culture March 26. 



Date 


Temper- 
ature ° F 


Number of 

red corpiis- 

cles per 

c. mm. 


Number 

of white 

corpuscles 

per 

c. mm. 


Remarks. 


Mar. 26 


106.2 


3,535,000 


18,940 


Well. 


Mar. 28 


110.0 


2,430,000 


70,000 


Fowl eats very little. 


Apr. 2 


110.6 


1,684,210 


80,000 


Blood very pale; fowl 
weak; refuses food. 


Apr. 3 


106.0 


1,745,000 


245,000 


Very weak; many red 
corpuscles attacked by 
leucocytes. 


Apr. 4 








Found dead. 



In stained preparations of the blood numerous red corpuscles are 
observed undergoing degeneration. This is manifested by the fail- 
ure of the cellular protoplasm surrounding the nucleus to stain reg- 
ularly or at all, and also by vacuolization of the protoplasm of the 
cell. 

Bacterium sanguinarium may be recovered in pure culture on arti- 
ficial culture media from the blood, liver, spleen and kidneys of 
fowls recently dead of the disease. 

Differential diagnosis. Fowl typhoid is distinguished from 
fowl cholera by the absence of severe congestion of the mucous mem- 
brane of the intestine especially the duodenum, by the absence of 
hemorrhagic spots on the heart, by the failure to find bipolar stain- 
ing bacteria in the blood, and by the finding and isolation of B. 



54 DISEASES OE DOMESTICATED BIEDS 

sanguinarium. Also, the duration of symptoms is apt to be mucli 
shorter in the case of cholera. 

Fowl typhoid is differentiated from fowl pest by the absence of 
severe intestinal congestion, failure to find petechise in the mucosa 
of the proventriculus and by the fact that fowl pest is caused by 
a filterable virus and no organisms can be detected in the blood 
stream, or isolated on artificial culture media. 

Infectious leukemia has somewhat similar lesions and also shows 
a greatly changed condition of the blood. However, in this disease 
the loss of red cells and increase of white cells is much more marked 
than in fowl typhoid. Also, it is the mononuclear cells, instead 
of the polymorphonuclears, which show the principal increase in 
numbers in infectious leukemia. Unlike fowl typhoid, infectious 
leukemia is caused by a filterable virus and no microorganism can 
be grown, from the blood or organs on artificial culture media. 

Fowl typhoid and acute Bacterium pullorum infection of grown 
fowls have symptoms and lesions which are somewhat similar. The 
causative organisms also closely resemble each other both morpho- 
logically and in their cultural characteristics. In B. pullorum in- 
fection, however, the ovary is congested and nearly always presents 
several hard irregular ova. It is the principal seat of predilection 
for the pullorum bacterium. 

PSITTACOSIS OF PAEEOTS 

Synonyms. Septic fever of the parrot, parrot septicemia, (Eng- 
lish) ; septicemic des perruches, mycose des perroquets, (French) ; 
Psittacosis, (German). 

Characterization. The disease is a contagious septicemia in- 
volving parrots and parrakeets and causing fever, weakness, stupor 
and diarrhea. 

Transmission to man. The disease has received considerable 
attention because suspicion has been aroused that the infection may 
be transmitted to man. A number of outbreaks of infectious pneu- 
monia in man have been observed to occur simultaneously with the 
bird disease. 

Leichtenstern sums up the question of the transmission of the dis- 
ease to man as follows : 

" 1. Epidemiological, clinical and especially bacteriological evidence is 
not disclosed to prove that the infection of house epidemics of pneumonia 
suspected of being psittacosis, did originate from sick parrots. 

" 2. It is proven that bacterial diseases, especially enteritis, occur fre- 



FOWL TYPHOID AND SIMILAR INFECTIONS 55 

quently in parrots, particularly those freshly imported, and inflict sporadic 
and also excessive mortality. 

" 3. No one will doubt that the streptococci, staphylococci, pneumococei, 
coli and proteus varieties occurring in these fatal parrot diseases may 
under certain circumstances also become dangerous for man. 

" 4. The disease of man designated psittacosis is in clinical and ana- 
tomical features an atypical pneumonia coupled with tyi^hoid symptoms 
and the disease has the same character in all epidemics. 

" 5. The same house epidemics of pneumonia occur not rarely, without 
the intervention of parrots and one may from this draw the conclusion 
that all the former psittacosis epidemics were nothing more than atjioical 
pneumonia in which the sick parrot, accidentally present in the house, 
played no etiological role. 

" 6. The above conclusions under 5 are contradicted in some measure by 
the no small number of former so-called psittacosis house epidemics. 
Especially contradictory to these conclusions is the Paris epidemic of 1892 
in which the transmission of the disease from the sick parrots to man 
must be considered on the basis of epidemiological facts as, at the least, 
apparently wholly indicated." 

Etiology. An organism belonging to the hog cholera group has 
been isolated from cases of the disease in parrots, by IsTocard and 
by Palamidessa. It is an actively motile, Gram negative rod which 
grows equally well under aerobic or anaerobic conditions. The 
gro^vtll in bouillon and on agar presents no characteristic features. 
Growth on gelatin at first consists of a shiny, transparent, iridescent 
streak which develops into a porcelain-white growth. 'No liquefac- 
tion of gelatin occurs, and milk is not coagulated. Growth on potato 
resembles that of B. coli. The organism may be isolated from the 
blood, bone marrow, spleen and other organs of infected birds. It 
has been isolated from the intestinal contents of parrakeets which 
were in apparent good health. 

Pathogenesis. The causative organism is pathogenic for the 
parrot, parrakeet, pigeon, fowl, mouse, rabbit and giiinea pig. All 
discharges of an infected bird are infective and in view of the close 
contact between birds there is every opportunity for transmission 
of infection. The disease occurs most frequently among birds dur- 
ing shipment from the tropics and shortly after landing. Contribu- 
tory factors to its occurrence seem to be the unusual restraint, crowd- 
ing, filthy cage conditions, climatic conditions and general hard- 
ships suffered during shipment. 

Symptoms. The disease is manifested by shivering, inappe- 
tence, diarrhea with frothy greenish droppings which are sometimes 
blocdv. The bird exhibits gTcat thirst, drowsiness and disinclination 



56 DISEASES OF DOMESTICATED BIEDS 

to move. The wings droop, the eyes are closed, the feathers are 
ruffled and the head is turned on the shoulder. When attempt is 
made to move, great weakness is evident. The bird usually avoids 
the perch. Convulsions precede death by a short period. In more 
chronic eases there is a discharge from the nostrils and eyelids, 
coughing, snuffling and difficult, panting respiration. Emaciation 
is evidenced by prominent breast bone and loss of weight. Vomiting 
is occasionally observed. 

The disease is usually fatal and hope of recovery may be enter- 
tained only in cases which survive for eight or nine days and which 
display some appetite. Most die in from three to five days after 
sickness is noted. 

The incubation period in natural exposure varies from three days 
to several weeks. 

Morbid anatomy. The organs of the abdominal cavity show 
intense congestion and ecchymoses are present in the peritoneum. 
Small grayish spots may be observed in the liver, spleen and kid- 
neys. The spleen is usually enlarged and soft in texture. The 
intestines show general congestion, or catarrh and often contain 
ulcers on the mucosa. The muscles often present a striated and 
spotted appearance. The heart muscle is often dark or hemor- 
rhagic. Ecchymoses may be present in the endocardium and peri- 
cardium. The lungs may present various conditions such as total 
consolidation, yellowish pneumonic patches, areas of atelectasis or 
of congestion. The air sacs may contain fibrinous or fluid exudate. 

Treatment. The patient sliould be kept in a room having a 
temperature of from 90° to 100° F. continuously. Gray advises 
that aspirin or cyllin may be given in the drinking water. In cases 
showing improvement, the aspirin may be replaced by aromatic sul- 
phuric acid and quinine sulphate. Food may consist of bread and 
milk, banana, sponge cake soaked in sherry, etc. 

Prevention. The most effective prevention would consist of 
improvement of methods of isolation of individuals and of general 
conditions on shipboard. Prophylaxis on shore involves perfect 
segregation of birds and the application of disinfection. 

DISEASE OF PIGEONS CAUSED BY A BACILLUS OF THE 
HOG CHOLERA GROUP 

Moore observed an infection in pigeons in ISTew Jersey caused by 
an organism closely related to Bacillus suipestifer. 



FOWL TYPHOID AND SIMILAR INFECTIONS 57 

Symptoms. The disease is characterized by emaciation and a 
peculiar turning of the head from one side to the other. Occasion- 
ally there are paroxysms of aimless flying about. The disease is 
popularly designated " megrims." 

Etiology. The organism belongs to the hog cholera group of 
bacteria but differs in several particulars from the specific organism 
isolated from affected hogs. The organism from the pigeon is ap- 
preciably larger. In bouillon a delicate pellicle develops on the 
surface of the fluid, and in old cultures, a deposit is formed on the 
sides of the tube. A marked indol reaction occurs. The pigeon 
culture is less rapidly fatal for experimental animals than B. sui- 
pestifer. 

Morbid anatomy. Autopsy of a bird that had slio^vn the pe- 
culiar head movement for several days revealed no lesions in the 
thoracic or abdominal cavities. There was a friable exudate about 
1 mm. in thickness, in the subarachnoid space over the cerebellum 
and the posterior lobes of the cerebrum. It was grayish yellow in 
color and easily removed. The subjacent brain tissue was reddened 
but otherwise the brain was normal in appearance. The organism 
in question was recovered in pure culture from the brain lesion but 
not from the heart blood. Another pigeon found dead, showed great 
emaciation but few other changes beyond pale, fatty heart nmscle. 
The same organism was recovered in pure culture from the liver and 
blood. 

AX INFECTION IN PIGEONS CAUSED BY BACILLUS PARATYPHOSUS B. 

Zingle observed an infection in pigeons apparently caused by B. 
jxira typhosus B. 

Morbid anatomy. The external appearance of the carcass, be- 
yond marked emaciation, presents nothing suspicious. The oral 
cavity in all cases is free from lesions. Upon skinning, the breast 
muscle is seen to be colored yellow in some places and permeated 
with bright yellow knots like oat gi-ains. The liver frequently has 
a yellowish gray color, and on closer observation it is seen to be cov- 
ered over the whole surface with countless hyperemic areas, which 
are sharply defined from the surroundings. In more cases the liver 
is permeated with yellow, round, compact knots varying in size from 
that of a grain of wheat to that of a bean, which give the surface a 
roughened appearance. The spleen is generally small without par- 
ticular macroscopic changes. The intestine appears somewhat hem- 



58 DISEASES OF DOMESTICATED BIRDS 

orrhagic. The most marked lesions are shown by the kidneys. 
These are extraordinarily large, and the borders of the several 
lobules have completely disappeared. The color of the kidneys is 
mostly gray-yellow. They appear to be sprinkled through with 
numerous speck-like foci and they are very fragile in consistency. 
The lungs appear free from lesions in many cases. Frequently, 
however, the lungs contain numerous opaque, gray-white foci the size 
of a hemp seed which are uniformly distributed. Lesions are not ob- 
served in the trachea, but the mucous membrane of the crop in iso- 
lated cases contains yellow crumbly, button-like areas of exudate. 

Etiology. In the bacteriological examination of blood, muscu- 
lature and organs a bacillus was found which agreed with paraty- 
phoid B in cultural, morphological and serological characters. The 
culture agglutinated in a dilution of 1 : 15,000 completely and par- 
tially at 1 : 25,000 wath B. parody phosus B serum of a titre of 
1:30,000. 

All the strains showed the same characteristics as B. paratyphosus 
B in litmus milk, glucose, Endo agar, malachite green agar, gelatin, 
Barsiekow solution 1 and 2, neutral red agar, orzein agar as well 
as milk, potato and bouillon. 

Pathogenicity. White mice succumbed to subcutaneous injec- 
tion in two days. It was especially noticeable that the organism 
occurred in great numbers, and was never observed mixed with 
other organisms. 

Pathological histology. In microscopic sections of the kidneys 
there are found inflammatory foci somewhat larger than a millet 
seed with round cell infiltration of the interstitial area. Also 
parenchymatous degeneration of the epithelium of the convoluted 
tubules in that the nuclei of the same in part are poorly stained and 
the protoplasm appears to be granular. The lumina of the tubules 
are filled with masses of desquamated epithelial tissue. When 
stained with Sudan they show fatty degeneration of medium degree 
in the epithelium of the labyrinths. 

The investigation of the liver shows that the organ is permeated 
with numerous abscesses. 

The knots in the musculature present themselves microscopically 
as abscesses varying in size from that of an oat grain to that of a 
pepper seed, with distinct lymphocyte walls which mingle with the 
neighboring muscle fibers. In the center of the abscesses there is 
much fibrin and also pus cells. 



FOWL TYPHOID AND SIMILAR INFECTIONS 59 

In the lungs there are numerous abscesses analogous in structure 
to those in the muscle. 

Relation to bird pox. Because of a suspicion that bird pox 
virus was present, inoculation experiments were undertaken. By 
rubbing of pus from liver, kidneys, lungs, etc., as well as blood and 
musculature, skin, muscle nodules, and crop exudate, into scarified 
breast skin of pigeons, there appeared after 2 to 3 days, yellowish 
swellings which looked exactly like pox. After a week they reached 
the maximum size of a pea. During this time the breast muscle fell 
away very markedly. These swellings began to shrink and dry up, 
while as a rule no fresh swellings appeared. Some of the pigeons 
died within 2 to 4 weeks after inoculation. By that time the pox- 
like swellings on the breast skin were totally dried up or had fallen 
off. The musculature was atrophied, flecked with yellow and in 
some cases contained numerous knots shaped like an oat grain with 
section findings like those in the original pigeons. 

Other pigeons lived. After some time the pox scabs fell off, the 
breast muscle filled out, so that the bird appeared clinically healthy. 

These results were obtained easily through inoculation of gener- 
ation after generation, also with dried out material, and the B. para- 
typliosus B could be recovered each time. 

The question arose as to whether these organisms were the pri- 
mary cause of this pigeon disease or whether like hog cholera, the 
paratyphoid bacillus played a part of a leader. There was the pos- 
sibility of a mixed infection with bird pox, and on this account ex- 
periments were started with contamination free filtrates of cultures 
and organs. 

Also inoculation experiments were undertaken with cultures that 
had been grown for many generations in fluid and solid media. 

While the filtrate experiments gave no positive result, inoculations 
with pigeon paratyphosus culture always gave pox-like appearances 
in two days. 

AVIAN SALMONELLOSIS 

Lignieres and Zabala describe an infection in fowls caused by an 
organism which they regard as showing all the specific characters of 
the hog cholera bacillus. The authors note that their organism is 
non-motile, while the hog cholera organism of Salmon and Smith is 
motile. However, they conclude that this difference is not sufiicient 
to differentiate the organisms. Consequently they propose the name 
avian salmonellosis for the disease observed. 



60 DISEASES OF DOMESTICATED BIRDS 

Etiology. The organism isolated is a non-motile rod wliicli is 
Gram negative. Whether a precipitation of casein occurs in milk 
or not, the medium becomes liquid again in 5 to 8 days. The color 
is grayish and the reaction is strongly alkaline. Indol is not pro- 
duced and gelatin is not liquefied. Growth occurs on potato. There 
is nothing distinctive about growth on other media. 

Pathogenicity. It is possible to inoculate healthy hens and rab- 
bits with several drops of infected blood without killing them. Sub- 
cutaneous inoculation with culture does not always kill hens but 
intravenous injection of 1 to 2 c.c. of culture has a fatal result. The 
pigeon is easily killed by intravenous and subcutaneous inoculation. 
Ducks and geese are resistant to the infection. The rabbit inocu- 
lated intravenously with 1 c.c. of culture is killed, while subcutaneous 
inoculation merely causes tumefaction at the point of inoculation. 

Symptoms. 'No symptoms characteristic of the infection in 
question are displayed. 

Morbid anatomy. The comb is black, and sometimes dark 
ecchymoses are observed on the skin. There is a clear fluid in the 
pericardium. The liver and the kidneys are congested. The spleen 
is enlarged and much more so than in fowl cholera. The mucosa 
of the digestive tract is reddened in places, but hemorrhages are 
rarely found. 

PATHOGENICITY OF B. ENTEEITIDIS AND B. PAEATYPHOSUS B 

TO BIRDS 

Reinholdt has found that introduction of either B. enteritidis or 
B. parafyphosus B into hens, pigeons, geese and ducks, sometimes 
causes a transitory disease and sometimes a fatal disease. This is 
true of a wide variety of methods of inoculation such as intravenous, 
intraperitoneal, subcutaneous and intramuscular injection, as well as 
administration by the stomach. Pigeons are most susceptible to in- 
fection, followed in order by geese and hens. Administration of the 
organisms per os under normal conditions of feeding is of least 
influence. A very large number of organisms is necessary to induce 
infection. The organisms are always recovered when the bird dies, 
but this is not always true when a bird is slaughtered while healthy. 
Agglutinins are detected six days after infection. 



FOWL TYPHOID AND SIMILAR INFECTIOXS 61 

SEPTICEMIAS CAUSED BY COLON BACILLI 

Fowls. Outbreaks of septicemic infections in fowls caused by 
B. coJi have been reported by Lignieres, Martel, Claussen, Zeiss and 
Sclilegel. 

The symptoms are practically indistinguishable from those of 
fowl cholera. The birds show somnolence, depression, diarrhea and 
inappetence. In the late stages, the comb may be dark colored as 
in cholera. 

At autopsy, there is inflammation of the intestines with hemor- 
rhages in places. There may be a small amount of serous exudate 
in the abdominal cavity. The spleen is softened and hypertrophied. 
There is pericarditis manifested either by the presence of hemor- 
rhages, solid exudate or fluid exudate. Microscopic examination of 
stained smears from the blood and organs shows numerous bipolar 
staining rods. However, the organisms average twice as large as 
those of fowl cholera. 

In inoculation experiments made by Lignieres, hens resisted sub- 
cutaneous and intramuscular injection of 1 to 2 c.c. of culture. On 
the other hand the pigeon succumbed to a dose of 1 c.c. The same 
dose injected subcutaneously into the rabbit and guinea pig caused 
only a local abscess, while intrapleural or intraperitoneal injection 
killed. 

Martel killed hens by intramuscular injection of small amounts 
of culture. Failure resulted from attempts to cause infection by 
intravenous injection or by ingestion of cultures, excrement and 
virulent products. The giiinea pig, rabbit, white rat and white 
mouse w^ere found to be susceptible to injections. 

Claussen isolated a strain that was uniformly fatal to canary 
birds, white mice and guinea pigs. Pigeons, hens and ducks became 
sick only exceptionally. The infection led to the death of only 50 
per cent of the inoculated birds, while the remainder recovered 
after three to six days. The incubation period was on an average, 
twelve hours long. Rabbits were very refractory to inoculation. 

Claussen concludes that colon organisms occurring in the intes- 
tines of healthy hens possess the ability of becoming virulent under 
certain conditions and cause a cholera-like infection. These spe- 
cial conditions are believed to be furnished by the harmful influ- 
ence exerted by shipment for long distances with resulting hunger, 
thirst, cold and lack of ventilation. 

Zeiss reports a case in which two hens in a healthy flock sud- 



62 DISEASES OF DOMESTICATED BIEDS 

denly displayed lack of appetite with depression and died soon. 
Autopsy revealed extraordinary softness of the spleen and liver to- 
gether with limited subcutaneous hemorrhages. Preparations from 
the blood revealed bipolar rods. The organism isolated from the 
cases showed the morphology and biologic characteristics of B. coli. 

The organism was pathogenic for canaries. On the other hand, 
guinea pigs could not be infected by either subcutaneous nor intra- 
venous injection with 2 c.c. doses of 24 hour bouillon culture. 

Pigeons. Sanfelice observed an outbreak of a disease among 
pigeons caused by B. coli. Most of the birds appeared at autopsy 
as follows: On opening the abdominal cavity a sero-fibrinous exu- 
date is noted on the whole surface of the intestines. The abdominal 
fluid is increased in amount. The spleen is swollen. There are 
adhesions of the intestines, the heart and the liver. The exudate 
appears in the form of a pseudomembrane in that when grasped 
with tweezers, it pulls off completely. In some pigeons besides the 
peritonitis described, there is inflammation of the mucosa of the 
oviduct, which is covered with a purulent exudate. Often eggs are 
found in the oviduct, which could not be laid on account of the 
inflammation. An organism identified as B. coli was observed in 
smears and was recovered in culture from the oro-ans. Pigeons 
inoculated subcutaneously with one to one and one half c.c. of cul- 
ture, developed an abscess at the point of inoculation but did not 
die. Larger doses injected into the abdominal cavity caused death. 

Pheasants. Klein described an organism isolated from young 
pheasants dead of an infectious disease. The organism was motile, 
somewhat shorter than B. coli and did not coagulate milk. He 
concludes that the organism, though belonging to the same family as 
B. coli, was a different species. 

GEOUSE DISEASE 

Under the name of grouse disease, Klein has described a pneu- 
monia caused by a member of the B. coli gi*oup. Subsequent inves- 
tigation by a committee of inquiry on grouse disease revealed the 
fact that the condition of the lungs described by Klein represents 
post-mortem changes. The supposed etiological agent is regarded 
by the committee as a post-mortem invader. It was noted that 
Klein had opportunity to study only birds that had been dead sev- 
eral days. The cause of mortality among grouse was watched by 
the committee very closely for six years and in no instance was 



FOWL TYPHOID AND SIMILAR INFECTIONS 63 

there observed an epizootic like that described by Klein. A large 
number of agencies are responsible for the death of grouse, and 
probably the most important is infestation with Trichostrongylus 
pergracilis as pointed out first by Cobbold. 

QUAIL DISEASE 

Synonym. Colibacillosis tetraonidarum. 

Characterization. Quail disease is an infectious disease which 
according to Morse is caused by a member of the colon group and 
characterized by congestion of the lungs, focal necrosis of the liver 
and ulceration of the intestine. It has been recognized only among 
birds in captivity. 

Species affected. The disease has been observed in the bob- 
white (Colinus virginidnus) , the California quail (Lophortyx cali- 
fornicus vaUicola), the Gambel quail (Lophortyx gamheli), the 
mountain quail (Oreortyx pidus), the scaled quail (Callipepla 
squamata) and the sharp-tailed grouse (Pediocaetes phasianellus 
canipestris) . 

History. The disease for many years has been observed among 
quail shipped for stocking areas of land and appears during trans- 
portation, or immediately after. It seems evident that the unusual 
conditions and hardships endured during the shipment constitute 
an important factor predisposing to the occurrence of the infection. 
Many outbreaks occur among quail which have been recently cap- 
tured in Mexico. Morse has written an article summing up the 
available information regarding the characteristics of the disease. 

Etiology. Morse reports finding a bacillus of the B. coli group 
present in diseased birds, with striking constancy. Cultures are 
readily isolated from the liver and intestines. It cannot always be 
cultivated from the heart blood of birds dead of the disease, nor 
always from the lungs. 

Pathogenesis. The organism is not pathogenic for chickens, 
pigeons nor rabbits but kills mice and guinea pigs with characteristic 
lesions. Experiments with quail are hindered by the difficulty in 
obtaining birds that have not been exposed to infection. 

Symptoms. The symptoms first become manifest by dullness, 
inappetence and ruffling of the feathers. Death may occur within 
two or three days after the appearance of symptoms. In chronic 
cases emaciation becomes extreme. 

Morbid anatomy. As a rule, the carcass is in good condition. 



64 DISEASES OF DOMESTICATED BIRDS 

There is slight congestion of the lungs, and of the liver. The sur- 
face of the latter organ presents a few areas of necrosis. Some- 
times the liver contains no necrotic spots and is merely congested, 
but in some cases the necrosis involves a large area. The intestinal 
wall contains numerous small yellowish areas of necrosis which may 
be seen through the peritoneal surface. These may be exceedingly 
minute, or reach the size of a pinhead. In some cases the necrotic 
process appears in the form of ulcers, some of which may perforate 
the intestinal wall. In other cases the intestinal lesions may con- 
sist of mere reddened areas. 

Prophylaxis. It is likely that the removal of birds from the 
natural wild environment, interference with natural food supply, 
crowding in cages and shipment are the fundamental factors pre- 
disposing birds to infection. These undesirable conditions of \\n- 
natural crowding are difficult to correct. 

The cleaning and disinfection of shipping cages should be carried 
out very thoroughly. So far as possible, birds should be isolated 
in small lots during shipment. All possible precautions to prevent 
the contamination of feed and water should be carried out. 

Treatment. The nature of the disease and subjects are such as 
to prevent successful treatment. 

asthenia in fowls 

(going light) 

Characterization. The affection is characterized by extreme 
emaciation associated with reddening of the walls of the duodenum. 

History. Dawson described the disease as occurring in the vi- 
cinity of Washington, D. C. 

Etiology. The organism isolated from the duodenum of af- 
fected birds is designated Bacterium aMheniece and is regarded as 
a variety of the colon species. 

Pathogenicity. Dawson was imable to induce disease in chick- 
ens by feeding organs or cultures, or by inoculating them intra- 
abdominally, subcutaneously and intravenously. ISTevertheless he 
was inclined to believe that the organism in question was the cause 
of the disease. 

Dawson considers that the presence of the organism in the part 
of the alimentary canal where the digestive process is most active 



FOWL TYPHOID AND SIMILAR INFECTIONS 65 

interferes with nutrition. Pigeons, mice and rats proved equally 
refractory. A guinea pig inoculated subcutaneously with duodenal 
contents succumbed to the infection. Rabbits inoculated subcutane- 
ously with culture and fed the same, proved refractory. Intra- 
abdominal inoculation of half a cubic centimeter of culture proved 
fatal to a rabbit. 

Symptoms. Extreme emaciation is the most noticeable symp- 
tom. The appetite is voracious. There is no evidence of diarrhea 
and no increase of temperature. The comb and wattles are slightly 
more pale than normal. 

Morbid anatomy. Autopsy of affected fowls reveals extreme 
emaciation of the muscular system and viscera with almost complete 
absence of fat. There is reddening of the walls of the duodenum 
and the contents are mucoid in appearance. 

Treatment. Dawson recommends purgation to remove the or- 
ganisms in the duodenum. For this purpose he administers castor 
oil in a dcse of two teaspoonfuls or calomel in one fourth grain doses 
repeated frequently. He suggests that purgation be followed by a 
stimulating tonic recommended by Megiiin as follows : Powdered 
fennel, anise, coriander seed, cinchona, each 30 grains ; powdered 
gentian and ginger, of each 1 dram; powdered sulphate of iron, 
15 gTains. Mix. Add from 2 to 4 grains of this mixture for each 
fowl to the food twice a day. 

REFERENCES 

1. Claussen. L^eber Kolibakterienseptikamie bei Hiihnern als Trans- 
portkrankheit. Ztschr. f. Ir^fehtionshr. d. Haustiere, Bd. 3, 1907, S. 69. 

2. Committee of inquiry on grouse disease. The grouse in health and 
disease. London : Smith, Elder & Co., 1911. 

3. Curtice. Fowl typhoid. Rhode Island Agr. Exp. Sta. Bull 87. 1002. 

4. Diipuy. De la psittacose au point de vue epidemiologique. Prog. 
Med.. 1897, p. 225. 

5. Hadley. Infections caused by bacterium ptdlorum. Rhode Island 
Agr. Exp. Sta. Bull. 172. 

6. Klein. Ueber eine akute infektiiise Krankheit des schottiscben Moor- 
huhnes (Lagopus scoticus). Centralhl. f. BaMeriol, Bd. 6, 1889, S. 36. 

7. Klein. Ein weiterer Beitrag zur Kenntniss des Bacillus der Grouse- 
disease, Cenfrolhl. f. Bal-ferioL, Bd. G. 1889, S. .593. 

8. Klein. T^eber eine epidemisclie Krankheit der Hiihner, verursacht 
durch einen Bacillus-Bacillus Gallinarum. Centralhl. f. Bal-teriol., Bd. 5, 
1889. S. 689. 

9. Leiehtenstern. Ueber infektiose Lungenentzundungen und den 



66 DISEASES OF DOMESTICATED BIEDS 

heutigen Stand der Psittacosis-Frage. — Werden durcli spezifish erkrankte 
Papageien bosartige Lungeneiitzundungen beim Menschen herv'orgerufen ? 
Centralhl. allgem. Gesundheitspfl., Bd. 18, 1899, S. 241. Abs. in Centralhl. 
f. Bakteriol {Etc.), 1. AU., Orig., Bd. 26, 1899, S. 651. 

10. Lignieres. Septicemie a coli-bacille chez la poule Compt. rend. 
Soc. de Uol., T. 46, 1894, p. 135. 

11. Lignieres and Zabala. Sur tine nouvelle maladie des poules. Bull. 
Soc. Cent, de Med. Vet., T. 59, 1905, p. 453. 

12. IVIartel. Maladie a coli-bacille de la poule et de la dinde. Compt. 
rend. Soc. de boil, T. 49, 1897, p. 500. 

13. Moore. On a pathogenic bacillus of the hog-cholera group associ- 
ated with a fatal disease in pigeons. U. S. Dep. Agr. Bur. Animal In- 
dust. Bull. 8, 1895. 

14. Moore. A study of a bacillus obtained from three outbreaks of 
fowl cholera. U. S. Dep. Agr. Bureau, Animal Indust. Bull. 8, 1895. 

15. Moore. Infectious leukemia in fowla — 'A bacterial disease fre- 
quently mistaken for fowl cholera. U. S. Dep. Agr. Bureau Animal In- 
dust. 12th and 13th Ann. Kep., 1895-96. 

16. Morse. Quail disease in the United States. TJ. S. Dep. Agr. Bureau 
Animal Indust. Circ. 109, 1907. 

17. Palamidessi. Di una infectione nell' womo transmesso probabilmenti 
dai pappagalli. Policlinico, 1895. Abs. in Centralhl. f. Bakteriol. (Etc.), 
1. AU., Orig., Bd. 20, 1896, S. 316. 

18. Pfeiler imd Rehse. Bacillus typhi gallinarum alcalifaciens und die 
durch ihn verursachte Hiihnerseuche. Mitteil. a. d. Kaiser Wilhelm In- 
stitnt f. Landwirthschaft in Bromherg, Bd. 5, 1913, S. 306; Abs. in Cen. 
train, f. BaUeriol. (Etc.), 1 AU. Ref., Bd. 58, 1913, S. 575. 

19. Pfeiler and Roepke. Zweite Mitteilung iiber das Auftreten des 
Hiihnertyphus und die Eigenschaften seines Erregers. Centralhl. f. Bak- 
teriol. (Etc.), 1 AU. Orig., Bd. 79, 1917, S. 125. 

20. Reinholdt. Infektionsversuche mit den " Fleischvergiftern " (Bacil- 
lus enteritidis Gartner und Bacillus paratyphosus B) beim Geflugel. Cen- 
tralhl. f. Bakteriol. (Etc.), 1. AU. Orig., Bd. 62, 1912, S. 312. 

21. Rettger and Koser. A comparative study of Bacterium pnllorum 
(Rettger) and Bacterium sanguinarium (Moore). J. Med. Research, Vol. 
35, 1917, p. 443. 

22. Sanfelice. Eine Seuche dei Tauben durch Bacterium coli verur- 
sacht. Ztsclir. f. Hyg. v. Infektionskr., Bd. 20, 1895, S. 23. 

23. Smith and Ten Broeck. Agglutination affinities of a pathogenic 
bacillus from fowls (fowl tyiihoid). (Bacterium sanguinarium, Moore.) 
/. Med. Research, Vol. 31, 1915, p. 503. 

24. Smith and Ten Broeck. The pathogenic action of the fowl typhoid 
bacillus with special reference to certain toxins. J. Med. Research, Vol. 
31, 1915, p. 523. 

25. Smith and Ten Broeck. A note on the relation between B. pul- 
lorum (Rettsrer) and the fowl typhoid bacillus (Moore). J. Med. Re- 
search. Vol. 31, 1915, p. 547. 

26. Taylor. A report upon an outbreak of fowl tj^phoid. J. Am. Vet. 
M. Ass., n. s. Vol. 2, 1916, p. 35. 



FOWL TYPHOID AND SIMILAR INFECTIONS 67 

27. Zeiss. Ivoliseptikiimie bei ITuhnern. Archiv f. Hyg., Bd. 82, 1914, 
S. 27. 

28. Zingle. Untersuchungen iiber eine Taubenseuche mit Paratyphus-B- 
Bazillenbefund. Zeitschr. Infehtionshr. d. Haustiere, Bd. 15, 1914, S. 269. 



CHAPTEK VI 

BACILLARY WHITE DIARRHEA 

Characterization. Bacillary white diarrhea is an acute, highly 
fatal septicemic disease of young chicks caused by Bacterium pul- 
lorum. The infection also exists in adult hens in a chronic, rarely 
fatal form, usually confined to the ovary. The disease as it occurs 
in hens bears no specific name and is merely referred to as B. pul- 
lomm infection. 

Etiology. Rettger and Harvey describe the characteristics of 
the organism substantially as follows : 

"Morphology, staining properties, etc. I'he organism is a long, slender 
bacillus (.3-5 micron x 1-2.5 microns) with slightly rounded ends. It 
usually occurs single, chains of more than two bacilli being rarely found. 
It is non-motile, non-liquefying, non-chromogenic, aerobic and facultatively 
anaerobic. In its microscopic appearances it resembles the bacillus of 
typhoid fever. It is stained readily by the ordinary basic anilin dyes. 
It does not stain by the Gram method; neither does it retain its color 
when treated with dilute acetic and mineral acids. The organism does 
not produce spores, or at least they have never been observed. 

" The maximum temperature tolerated is 56 to 57° C. (moist) for an 
exposure of fifteen minutes. The optimum temperature is 35 to 37° C. 

"Cultural characters: Agar plates. Small white colonies make their 
appearance within twenty-four hours. They increase in size slowly and 
seldom attain more than one millimeter in diameter, even after three or 
four days' incubation. Under themicroscope they appear yellow and vary 
in form from oval and spindle-shaped to round. The surface is usually 
marked with a rosette figure or what seems to be a lobed nucleus. Occa- 
sionally two or even three of these markings may be seen. 

" Slant agar. Growth is quite visible in twenty-four hours, and re- 
sembles that of the tyi^hoid bacillus. It spreads little and remains deli- 
cate, even after prolonged incubation. On glycerine agar the growth is 
practically the same. 

" Gelatin plates. Small white colonies may be seen in forty-eight hours. 
They remain small for several days, and only under exceptional conditions 
do they develop into characteristic surface colonies which to a certain ex- 
tent resemble the grape-leaf colony of B. typhosus. 

" Gelatin stah. A delicate growth occurs in forty-eight hours along the 
whole line of inoculation. It is of distinctly granular appearance and 
spreads very little on the surface. The gelatin is not liquefied. 

" On potato development is very slow. A narrow, almost invisible 

68 



BACILLAKY WHITE DIAKRHEA 69 

streak is produced along the line of inoculation. In litmus milk little or 
no apparent change occurs within the first forty-eight hours, after which 
the milk becomes slightly acidified without any signs of coagulation of 
the casein. 

" Gas production in sugar houillon. Negative results were obtained 
with maltose, lactose, saccharose, inulin, and dextrin bouillon. Dextrose 
and mannite were attacked, however, with both acid and gas production. 
In the dextrose fermentation tubes about twenty per cent of the closed 
arm was filled with gas, and the mannite tubes averaged about the same. 
The gas consisted of Co., and H in the ratio of 1 : 3. 

" Indol and nitrite production. Neither indol nor nitrite could be de- 
tected in Dunham's peptone solution at the end of one week's growth in the 
incubator." 

Toxin production. B. pullorum lias been shown by Smith and 
Ten Broeek to prodnce a toxin fatal to rabbits. Filtrates of bonillon 
cultures when injected intravenously may cause death Avithin two 
hours, or marked dyspnea followed by death over night, or cause loss 
of weight followed by recovery. The lesions induced, include con- 
gestion of various organs such as liver, spleen, kidneys, adrenals, 
lungs and mesenteric lymph glands together with hemorrhage into the 
gastric mucosa. 

Source of infection. Infection may occur in several ways. 
The most common source is through infected eggs. It has been 
demonstrated that affected chicks which survive the disease fre- 
quently retain the causative organisms in the system and later, in 
the event that the ovaiy becomes infected, pass them off in the eggs. 
Many infected eggs fail to hatch, the embryos dying in the shell at 
an early or late stage of development. Should one or more chicks 
be hatched, harboring the disease, the others of the lot are exposed 
early and nearly all become affected. The chicks are especially 
susceptible during the first 48 hours of life, but are practically in- 
susceptible after the third day. Another source of infection is 
through brooders and incubators that have previously held infected 
chicks. Day-old chicks frequently carry the disease to other points 
and contaminate brooders or infect other chicks with which they 
come in contact. However, the largest percentage of outbreaks is 
traced directly to the presence of infected hens in the flock from 
which the eggs for hatching were derived. There is a well defined 
cycle through which the bacterium passes ; namely, from the in- 
fected ovary of the hen through the egg to the chick and back to the 
ovary of the pullet which has survived the disease as a chick. 

Pathogenicity. Susceptibility to infection bears a remarkable 



70 



DISEASES OF DOMESTICATED BIRDS 




relation to age. During the first fortv-eigiit hours the baby chick 
is most susceptible to Bacterium pullorum and at this period of life, 
has practically no resistant forces to combat the infection. In the 
succeeding twenty-four hours, more resistance is shown bv those not 



BACILLARY WHITE DIARRHEA 71 

previously affected. At the end of four days, the unattacked chicks 
have generally acquired a resistance to acute infection. The re- 
sistance at this age, while very apparent in broods of young chicks, 
is not absolute, since fatal outbreaks in old fowls are recorded in the 
literature on the disease. 

Half grown guinea pigs are killed in from 24 to 48 hours when 
injected subcutaneously. The chief lesion is a large edematous area 
beneath the skin of the abdomen. Rabbits are killed in three to 
seven days by subcutaneous injection of one to two c.c. of 48 hour 
bouillon culture. In the case of all experimental inoculations, the 
organism may be recovered in pure culture from all the internal 
organs. 

Mortality. Baeillary white diarrhea is, without doubt, the most 
fatal disease of young chickens. i\jnong those broods affected, the 
death rate varies between 40 and 90 per cent. The high percentage 
is UK^-e often registered than the low one. 

Symptoms. The external symptoms of baeillary white diar- 
rhea are similar to those of coccidial and aspergillar white diarrhea. 
The presence of soft, whitish droppings and similar symptoms in 
each case caused these three diseases to be grouped under the com- 
mon term " white diarrhea." The position of each as an important 
specific disease requires that they should be treated separately, espe- 
cially since they are not confined to young chicks but affect gro\vn 
fowls as well. 

The affected bird is drowsy, and dejected in appearance. The 
feathers are rufiled, the wings droop and the chick sways back and 
forth in a standing position. The appetite is diminished. The 
irritation of the droppings when being voided often causes the 
chick pain as evidenced by a peculiar cry at the time. The drop- 
pings may adhere to the down about the vent, blocking the opening. 
This gives rise to the expression " pasting up behind." In acute 
cases the chick soon falls to the floor and death occurs after a short 
period of coma. In more chronic cases the chick remains standing 
in a dull inattentive position a good portion of the time while not 
under the hover or hen. It acquires the appearance of having a 
short back and a large abdomen. Often one or both feet swell. 
The chick stands on one leg with the toes of the elevated foot just 
touching the floor. Lameness is shown in attempts to w^alk. 

The disease may show itself within two or three days after the 
chicks are hatched and spread rapidly through the brood. The 
period of incubation is four to ten days. Deaths begin to occur 



72 DISEASES OF DOMESTICATED BIRDS 

soon after hatching and continue to the third or fourth week. 
Chicks which survive, remain stunted and unthrifty for some time. 

Morbid anatomy. The lesions observed on autopsy are not 
clearly distinctive for this disease which is purely septicemic in 
nature. The early, rapid development of the disease, in a host 
unprepared to combat it, prevents the formation of many distinctive 
lesions. The failure of the yolk to be absorbed is the principal 
abnormal condition that is apparent. However, this condition is 
observed in very young chicks which have died through other causes, 
such as weak constitution, faulty incubation, and brooder defects. 
The liver usually shows an ochre color, with bands or streaks of 
congestion. This appearance is not constant as in some cases an 
apparently normal mahogany or chocolate colored liver is observed. 
In some instances the liver has the normal appearance, and the yolk 
sac has been absorbed. This is especially common in less acute 
cases. The lungs may show minute necrotic areas and, as a rule, 
congestion. 

Diagnosis. Diagnostic features of the disease are its early 
appearance, the high mortality within the first month, the occurrence 
of deaths within a few days after hatching, and the absence of inter- 
nal lesions other than unabsorbed yolk or striations on the surface of 
the liver. Confirmatory positive evidence is obtained by examina- 
tion of stained smears of the blood, liver or yolk with discovery of the 
causative organism. Further evidence is yielded by feeding or in- 
oculation experiments with young chicks. 

Artificial cultural methods are more precise. The causative or- 
ganism may be readily isolated in a pure culture from the heart 
blood, liver, spleen, kidneys or unabsorbed yolk. It may be differ- 
entiated from other organisms of a similar type by its cultural and 
biochemic characteristics, and by its agglutinating properties against 
a homologous serum. 

Differential diagnosis. Bacillarv white diarrhea is differenti- 
ated from the other diseases commonly classed as white diarrhea by 
its early occurrence, the exceptional mortality, and the absence of 
the characteristic lesions of coccidiosis, or of aspergillosis. Coccidi- 
osis is slower in its development and usually affects chicks at a later 
period. It is manifested by hemorrhagic areas in the ceca, dilatation 
of these organs, and the presence of necrotic casts in their lumina. 
In the event that this disease is present, the coccidial cysts may be 
readily demonstrated on microscopic examination of the cecal con- 
tents. 



BACILLARY WHITE DIARRHEA 73 

Aspergillosis is comparatively rare in young chicks. Its charac- 
teristic growth may be found in the air passages, and the mycelia, 
or spores of the fungais can be observed by microscopic study of the 
moldy gTowth. 

Treatment. Attempts to cure bacillary white diarrhea are fu- 
tile. Some recover, owing to natural resistance, or other reasons. 
The so-called treatments recommended by some advisers are not to 
be relied upon. Once the disease has become established in the sys- 
tem, the causative microorganisms are distributed through the vari- 
ous organs by way of the blood stream and a septicemia has developed 
which is beyond the reach of any antiseptic treatment which has yet 
been discovered. By careful nursing, certain individuals might be 
assisted in surviving ; however, this is inadvisable because of the fact 
that the monetary value of the baby chick does not justify the ex- 
penditure of the time devoted to its treatment. Furthermore, the 
fact that those which recover are likely to serve as reservoirs for the 
causative organisms and constitute the sources of future outbreaks 
would speak against the policy of treatment. 

Where the disease is known to exist in a flock of breeding fowls 
and is anticipated in the hatch of baby chicks, precautions may be 
taken to lessen its attack by advanced treatment of the chicks. ^ Per- 
manganate of potash may be placed in the drinking water in sufficient 
quantity to give the latter a deep red color.^ This corresponds to dilu- 
tion of approximately 1 to 10,000. In such dilution, the antiseptic is 
non-irritating to the sensitive mucous membranes of the chick and 
may serve to inhibit the growth of the pullorum bacterium in contami- 
nated drinking water, and in the digestive tract of the chicks. But- 
termilk may be used as a food, as it combats the development of 
the bacterium in the intestine, due to the lactic acid which it 
carries. 

Prevention. The first principle of prevention is the eradication 
of carriers in the breeding stock, or the use of eggs for hatching 
which come from flocks known to be free of pullorum infection. 
Certain tests which are later discussed may be depended upon to 
detect the presence of the disease in a large percentage, if not all, 
of the infected hens of a flock. These birds may be discarded for 
breeding purposes or disposed of as the owner may desire. In this 
connection, it has come to our attention indirectly that in rare in- 
stances normal hatches have succeeded ones in which high mortality 
has occurred, the eggs in each case being derived from flocks in which 
a number of infected hens have been detected but retained as breeders. 



7-t DISEASES OF DOMESTICATED BIEDS 

The significance of this is not apparent, but opens an interesting field 
for study, if the observations are accurate. 

If it is desired to breed from an infected flock for the purpose of 
perpetuating the particular strain of fowl, or for other reasons, pre- 
caution may be taken to minimize the losses by the following pro- 
cedure. Incubator trays, or shelves, of the pedigree type which are 
partitioned oft" into compartments capable of inclosing a few chicks, 
say from six to ten as the owner may decide, are to be used. The 
partitions are to be sufiiciently high to prevent the chicks in adjacent 
compartments from coming in contact. This also means that the 
partitions should be of solid structure to prevent picking back and 
forth. It is only necessary to use such trays a day or two before 
the hatch is expected to come oft', and for three daj's after it is com- 
pleted. The chicks are to be retained in their respective compart- 
ments and need not be fed for 48 or even 72 hours, since they are 
provided with food material during this period through the yolk 
which is drawn into the abdominal cavity previous to hatching. 
Should symptoms of disease develop, the chicks in the particular 
compartment are to be removed and disposed of. The attendant 
should then disinfect his hands before watering or caring for the 
others. As the disease is contracted principally during the first 48 
hours of life, and only to a slight extent during the succeeding 24, 
this method of procedure will prevent a general spread to the hatch. 
The temperature and air requirements may be regulated to suit the 
needs of the chicks. Humidity, due to close confinement and lack 
of air circulation, is to be gTiarded against. The trays may be re- 
moved to the brooders, or similar structures may be placed in the 
latter and the chicks transferred to them, with care to avoid mixing 
the segregated lots. After three days, the danger of infection is re- 
duced to a minimum, and all of the hatch may be allowed to run 
together. 

BACTERIUM PULLORUM INFECTION OF GROWN FOWLS 

Occurrence. Infection of hens by the organism in question is 
not marked by external changes nor is it regarded as a common 
cause of death. Jones reports one outbreak due to B. pullorum in- 
fection which assumed an acute character with marked symptoms and 
considerable mortality. In this case the fowls were infected through 
the feeding of eggs which had failed to hatch and which came from 
an infected flock. About 50 birds died durino- the outbreak. The 



BACILLARY WHITE DIARRHEA VO 

present writers have encountered at autopsy a naturally infected 
fowl which had developed fatal B. pullorum septicemia from primary 
ovarian infection. 

Symptoms. In the chronic form, no symptoms are apparent to 
the observer. The fowls continue to lay, although from the number 
of retained and undeveloped ova, it is evident that laying is retarded. 
In the acute cases reported by Jones, within a period varying from 
two to six weeks after exposure by feeding, the affected birds showed 
a loss of appetite and energy. They appeared droopy and somnolent, 
with ruffled feathers and retracted heads. The combs and wattles 
were pale and more or less diarrhea was present. In the fatal cases, 
death ensued in from one to several days after the onset of symptoms. 

Morbid anatomy. In the acute cases autopsied by Jones the 
most constant lesions were the presence of small necrotic foci in the 
liver, spleen, pancreas and heart. The capsule of the liver, the peri- 
cardium and the heart were in many instances covered by a fibrinous 
exudate. 

In the majority of chronic cases, autopsy will show^ the lesions to 
be confined to the ovary. This organ usually presents an appear- 
ance quite characteristic. The diseased ova which have partially or 
wholly developed are hard, shrunken and angular. The natural yolk 
color has changed to a dark brown or greenish color. On cut section 
the ova are of a tough cheesy consistency, with a yellowish red, or 
greenish tinge. The condition of the ova closely resembles " gan- 
grene of the ovary " of earlier writers. The morbid ova may also 
appear as cysts, with darkened fluid contents. Occasionally only 
small cysts are present in the ovary and it is through cultural meth- 
ods alone that the presence of pullorum infection may be detected. 
Small foci consisting of sac-like structures with yellowish colored 
solid or fluid contents may occur in almost any portion of the ab- 
dominal or pleural cavities. Involvement of the pericardial sac is 
not uncommon. 

The causative bacterium may be readily isolated from the angular 
ova or cysts and grown on artificial culture media. In some cases 
where ovarian lesions are not pronounced, it is necessary to remove 
the ovary and disintegrate aseptically. The mass is placed in a 
flask of houillon, from which cultures may be plated on agar and 
the organism isolated in pure culture. 

Diagnosis. Several methods of diagnosing the presence of B. 
pullorum in fowls are available and are more or less satisfactory. 
The presence of bacillary white diarrhea in a brood of chicks which 



76 



DISEASES OF DOMESTICATED BIRDS 




Fig. 5. Xormal ovary. (Redrawn from Eettger, Kirkpatrick and Jones) 

has been batched from eggs from a particular flock of bens is proof 
enough of infection in the flock, providing that there is a reasonable 
certainty that contamination has not been introduced by outside 
sources or from infected incubators or brooders. Detection of the 
characteristic pullorum-infected ovaries, on post mortem examina- 
tion, is definite proof that the disease is prevalent in the flock. Bac- 




FiG. 6. Ovary infected with B. pulloriim. (RedrawTi from Rettger, Kirkpatrick 

and Jones) 



BACILLAEY WHITE DIAREHEA 77 

teriological examination of eggs from a suspected flock also leads to 
a diagnosis. However, this method is impractical because of the 
fact that an infected hen only occasionally drops an infected egg and 
considerable laboratory work is necessary to establish the presence of 
the disease. For the detection of individual carriers among hens 
held for breeders, two other methods which give positive proof of the 
presence of infection in the flock and pick out the infected individuals 
with a high degree of accuracy have been developed. These are the 
agglutination test applied first by Jones, and the intradermal test 
developed by the authors. 

Agglutination test. This test is based on the fact that the blood 
serum of an animal which has experienced the attack of a given 
species of bacteria will in some instances cause the organisms to 
agglutinate or form into clumps when a suspension of the bacteria 
is mixed with the serum of the animal in proper dilution. 

The wing vein is severed at the point where it passes over the 
elbow joint and 3 to 5 c.c. of blood collected in a sterile test-tube or 
vial. The flow of blood is then stopped by momentary pressure over 
the cut, or by the application of a small pledget of cotton. Usually 
no effort is necessary to stop the flow of blood, as chicken blood clots 
readily. Blood may be drawn more rapidly by severing the promi- 
nent vein visible on the ventral surface of the wing near the shoul- 
der. The collected sample is set aside and allowed to clot. It 
should not be agitated while the clot is forming, as this tends to 
prevent the collection of a clear serum. After the clot has formed, 
the sample may be placed in a refrigerator or other cool place. In 
a few hours the serum will have been pressed out by the contraction 
of the fibrin and can be drawn off as a clear fluid, free of blood cor- 
puscles or hemoglobin. If the test is not to be made immediately, 
the serum may be preserved by the addition of carbolic acid in suf- 
ficient quantity to form a .5 per cent solution. For this purpose, 
it is convenient to use a 5 per cent solution of carbolic acid as a 
standard, .1 c.c. being added to .9 c.c. of serum, or 1 drop to 9 drops. 
For the test a standardized suspension of B. puUorum is prepared. 
This may be heated at 60° C. for one hour, to kill the organisms, or 
used in the live state. The latter has been the practice of the au- 
thors. However, there appears to be no marked advantage in the 
use of live antigen, and killing by heat or .5 per cent carbolization 
has the advantage that the organisms are dead and hence absolutely 
harmless. 

In the test, the bacterial suspension is placed in the test tubes 



78 DISEASES OF DOMESTICATED BIRDS 

in the quantity of 1 c.c. to each tube. A series of tubes is em- 
ployed for each serum, depending on the number of serum dilu- 
tions to be made. In practice, a serum which causes agglutination 
in a dilution of .01 or even .02 is sufficient to establish a positive 
diagnosis. Using 1 c.c. as the standard amount of bacterial sus- 
pension, sera which have been diluted by the addition of normal salt 
solution to the extent of .04, .02, and .01 per cent of the original, 
are distributed in their respective tubes in quantities of 1 c.c. each. 
The tubes are labeled to show the identity of the various sera and 
the dilutions. In practice, it is found convenient to dilute the serum 
to 10 per cent of its original volume and add .4, .2, and .1 of a c.c. 
to the 1 c.c. of bacterial suspension. The tubes are shaken to insure 
a thorough mixture of the contents and may be set aside at a tem- 
perature of 37° C. for from twenty-four to forty-eight hours, when 
readings may be made. Instead, when rapid diagnosis is desired, 
they may be placed in an incubator at 37° C. for ^ hour and then 
centrifuged at the rate of 1500 to 1800 revolutions to the minute for 
several minutes. Either course gives similar results. In positive 
cases the organisms in the fluid collect in flocculent masses which 
have a tendency to form a diffuse coating over the bottom of the tube, 
while in the negative cases the organisms are deposited in a small 
circular mass in the center of the bottom of the tube. This is par- 
ticularly apparent where centrifugalization has been employed. On 
shaking the tubes the clearly positive ones will show a clear fluid 
containing flocculent masses while the negative ones are uniformly 
clouded. 

The agglutinating serum dilution which will establish a diagnosis 
has not been definitely fixed. It is a well known fact that normal 
blood serum is capable of agglutinating organisms to a greater or 
less degree. In B. pullorum infection tests, a serum which in the 
amount of .02 c.c. or less causes agglutination, undoubtedly indicates 
a positive case. 

Intradermal test. This test depends for its results upon the 
principle underlying allergic reactions. It is very similar in char- 
acter to the intradermal tuberculin test, especially as used to detect 
tuberculosis in fowls. 

A culture of several strains of B. puUorum from widely separated 
sources is growm in bouillon at a temperature of 37.5° C. for a 
period of thirty days to three months. Whether these time limits 
are necessary has not been determined. The product is then steril- 
ized at a temperature of 60° C. for a period of one hour and carbolic 



BACILLAEY WHITE DIARRHEA 



79 




acid is added in sufficient quantity to form a .5 per cent solution 
for preserving purposes. In the earlier experiments of the authors, 
the product was passed through a Berkefeld filter and concentrated 
to onc-tonth of its original volume. Later it was found that the 
original sterilized product concentrated to Vs its volume gave as 
satisfactory results. 

The material is injected into either wattle of the fowl in the 
amount of approximately .2 .^a^^?'?'*!;" 

c.c. The injection is made 
with a hypodermic syringe 
graduated in tenths of a c.c, 
and a needle of fine caliber 
is used to avoid causing 
traumatic swellings. The 
injection is made at a point 
near the lower border of the 
wattle. Where the flock is 
apparently free of infec- 
tious disease, no disinfect- 
ants are employed at the 
point of injection since the natural resistance of birds to ordinary 
wound infection is sufficient to giiard against infection. In the ab- 
sence of a graduated syringe, the amount to be injected may be 
gauged by injecting enough to cause a perceptible swelling at the 
point of inoculation. During the first three hours after injection 
the wattle shows an edematous condition which rapidly disappears in 
non-reacting birds. Ecadings are taken at twenty-four to thirty 
hours after injection. The wattle may be swollen to several times 
its natural thickness and may be readily observed at a distance, or 
the swelling may be so slight that palpation, or comparison with the 
uninjected wattle will be necessary. Any swelling other than that 
due to traumatism as a result of faulty technique, should be consid- 
ered significant. 

REFERENCES 



<;;;5gVti-V 



Fig. 7. Edematous swelling of wattle in- 
dicating positive reaction to the intrader- 
mal test for B. pullorum infection. 
(Original) 



1. Bushnell and Maiirer. The use of milk cultures of B. bulgarieus in 
the prevention and treatment of bacillary white diarrhea of young chicks. 
Am. Vet. Rev., Vol. 44, 191.3, p. 195. 

2. Gage and Martin. Notes on the histo-patholog>^ of the intestines in 
young chicks infected with bacterium pullorum. J. Med. Besearch, Vol. 
34, 191G, p. 149. 

3. Gage and Hyland. On the diagnosis of infection with bacterium 



80 DISEASES OF DOMESTICATED BIRDS 

pullorum in the domestic fowl. Mass. Agr. Exp. Sta. Bull. US, 1914. 

4. Gage and Paige. Bacillary white diarrhea (Bacterium pullorum in- 
fection) in young chicks in Massachusetts. Mass. Agr. Exp. Sta. Bull. 16S. 
1915. 

5. Jones. The value of the microscopic agglutination test in detecting 
fowls that are harboring Bact. pullorum. J. Med. Research, Vol. 27, 
1913, p. 481. 

6. Jones. Further studies on bacillary white diarrhea in young chickens. 
Rept. N. Y. State Vet. Col. 1910-1911, p. 69. 

7. Jones. An outbreak of an acute disease in adult fowls, due to Bact. 
pullorum. J. Med. Research, Vol. 27, 1913, p. 471. 

8. Rettger. Septicemia among young chickens. N. York M. J.. Vol. 
71, 1900, p. 802. 

9. Rettger. Septicemia in young chickens. N. Yorh M. J., Vol. 73, 
1901, p. 267. 

10. Rettger. Further studies on fatal septicemia in young chickens or 
" white diarrhea." J. Med. Research, Vol. 21, 1909, p. 115. 

11. Rettger. Ovarian infection in the domestic fowl and direct trans- 
mission of the disease to the offspring. J. Exper. M., Vol. 19, 1914, p. 552. 

12. Rettger and Harvey. Fatal septicemia in young chickens, or " white 
diarrhea." /. Med. Research, Vol. 18, 1908, p. 277. 

13. Rettger, Hull and Sturges. Feeding experiments with Bacterium 
pullorum. The toxicity of infected eggs. J. Exper. M., Vol. 23, 1916, 
p. 475. 

14. Rettger, Kirkpatrick and Card. Chickens: Milk feeding and its 
influence on growth and mortality. Comparative study of the value of 
sweet and sour milk. Storrs Agr. Exp. Sta. Bull. 80, 1915. 

15. Rettger, Kirkpatrick and Stonebiirn. Bacillary white diarrhea of 
young chicks. Third report. Storrs Agr. Exp. Sta. Bull. 7^. 1912. 

16. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young 
chicks. Fourth report. Storrs Agr. Exp. Sta. Bull. 77, 1914. 

17. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young 
chicks. Storrs Agr. Exp. Sta. Bull. 85, 1915. 

18. Rettger, Kirkpatrick and Jones. Bacillary white diarrhea of young 
chicks — VI. Storrs Agr. Exp. Sta. Bull. 88. 1916. 

19. Rettger and Stoneburn. Bacillary white diarrhea of young chicks. 
Storrs Agr. Exp. Sta. Bull. 60. 

20. Scherago and Benson. Experiments on the intradermal test for 
Bacterium pullorum. Cornell Yet., Vol. 9, 1919, p. 111. 

21. Ward and Gallagher. An intradermal test for Bacterium pullorum 
infection in fowls. TJ. S. Dep. Agr. Bull. 517. 



CHAPTER VII 

FOWL PLAGUE 

Synonyms. Bird plague, fowl pest, bird pest, infectious peri- 
tonitis of birds, exudative typhus of birds, Brunswick bird plague ; 
Peste aviarire, Peste des oiseaux (French) ; Geflilgelpest, Huhner- 
seuche, Huhnerpest, Vogelpest, Geflugelseuche, Kyanolophiea gallin- 
arum, Putenseuche (German) ; Peste aviaria, Epizoozia tifoide dell 
pollame, Tifo essudativo del gallinacei (Italian). 

Characterization. Fowl plagiie is an acute infectious disease 
of birds, caused by an ultra microscopic virus. It runs a rapid 
course and causes high mortality. 

Geographical distribution. The disease has been reported in 
Italy, Germany, France and Belgium. 

Etiology. The virus is ultra microscopic, passes through porce- 
lain filters, and is believed to be a protozoan. The presence of the 
virus has been demonstrated in the blood, the nervous system, nasal 
and oral discharges, serous exudates and feces. 

The virus is believed to be largely localized in the red blood cor- 
puscles. The virulence of the red corpuscles is such that death has 
been produced by a dose of .000,000,000,163,84 c.c. 

Dessication is not rapidly fatal to the virus for it has been ob- 
served to remain active for several weeks. It has been rendered 
inactive by exposure to direct sunlight or to a temperature of 65° 
to 70° C. for a few minutes. The activity of the virus is destroyed 
rapidly by whitewash and the common disinfectants. 

Certain granules have been observed in the brain of geese, hens 
and pigeons dead of the disease. Ottolenghi believes that they are 
derived from the nuclei of the cells. Certain peculiarities suggest 
to him the supposition that they contain the virus of fowl plague. 
Other granules in the brains of geese and hens are differentiated 
from the former by the fact that the cytoplasm of the cell is involved 
in their formation. 

Pathogenicity. The disease has been observed in fowls, turkeys, 
peafowls, giiinea-fowls, geese, pheasants, pigeons, ducks, and a large 
number of wild birds. Wild ducks when placed under conditions 
of semi-domestication contract the infection. 

81 



82 DISEASES OF DOMESTICATED BIRDS 

The virus is believed to be transmitted naturally by nasal and 
oral secretions, by the droppings of diseased birds or by eating 
carcasses of dead birds. Wounds of the skin when contaminated 
with virus readily result in infection. Mites (Dennanyssus avium) 
have been tested as to their ability to transmit the disease, with nega- 
tive results. Likewise ticks have given negative results. 

The disease is most frequent in early spring, declines in preva- 
lence in the summer and does not occur during the winter. In arti- 
ficial transmission, fowls succumb to subcutaneous or intramuscular 
injection or to application of the virus to the scarified skin. They 
likewise become infected by ingestion. 

After the subcutaneous or intramuscular injection of moderate 
amounts of heart blood and pieces of spleen or kidney the size of 
a pea the inoculated hens die as a rule within 36 to 48 hours, often 
in 3 to 4 days, and quite rarely only after 5 to 7 days. Feeding of 
larger amounts of pieces of organs causes death after about the same 
length of time or a few hours longer than in the case of subcutane- 
ous injection. Filtrates of nasal mucus, contents of the small in- 
testine, bile, brain, blood and internal organs are infective for hens. 
Many authors have failed to transmit the disease to old and young 
ducks or to young pigeons. Young geese are susceptible to sub- 
cutaneous and intramuscular inoculation or by the mouth, and die 
as a rule after about seven days. On the other hand, old geese 
are very slightly susceptible to ordinary methods of inoculation. 
Subdural inoculation of these has succeeded, and caused the nervous 
type of the disease. 

The disease exhibits peculiarities in showing a preference at dif- 
ferent times for different species of birds all in contact with one 
another, such as fowls, pigeons, geese and ducks. Mammals are 
immune to infection. 

In young geese and in pigeons the disease assumes the nervous 
type, which runs a much less rapid course. In these the virus at 
first localized in the blood corpuscles seems to disappear therefrom, 
and becomes established in the central nervous system. However, 
the virus may reappear in the blood shortly before death. 

Cominotti has obser\'ed the nervous type of the disease in wild 
ducks in confinement under conditions resembling those under which 
domesticated birds are kept. The virus was found always in the 
central nervous system and was never demonstrated in the blood or 
the internal organs even when large quantities of inoculating mate- 
rial were used. Transmission of the infection from w^ild ducks to 



FOWL PLAGUE 83 

fowls was possible bv subcutaneous injection of portions of cerebral 
svibstance. It was not possible to infect domesticated ducks with 
wild duck virus in doses however large, and administered by intra- 
venous inoculation, ingestion, intracerebral inoculation or instilla- 
tion into the conjunctivae. 

Symptoms. The incubation period is usually 3 to .5 days, but 
exceptionally 2 days or even 1 days. It is much shorter when birds 
are inoculated. The symptoms greatly resemble those of fowl chol- 
era. Death may occur while the bird is on the roost or on the nest 
without its having previously exhibited symptoms. 

There is an acute type of the disease in which the bird lives at 
the most three or four days. In a subacute form the birds survive 
7 or 8 days. Recovery practically never occurs. 

In the acute type, the first noticeable symptom is inappetence. 
Then the bird declines into a condition of weakness and somnolence, 
hides in corners, becomes indifferent to surroundings, with half 
closed eyes, drooping comb, and ruffled feathers. The temperature 
rises to 110° or 112° F., but may drop to subnormal before death. 
The comb commonly takes on a violet color which proceeds from the 
borders, or spots form on the sides, but it soon appears black. In 
some cases the comb is covered with white scales. The bird gen- 
erally dies quietly in a somnolent condition, which is only occa- 
sionally interrupted by spasms. 

In the subacute form which occurs quite frequently in cases of 
natural infection, the bird ceases to eat and drink, and goes on 
the nest for protection from the light. The general appearance is 
deceptive as indicative of the diseased condition. Upon investiga- 
tion and when an effort is made to see the bird walk, it may not 
rise to the feet, or moves the feet with difficulty, staggers, with the 
head wabbling and turned backwards which attitude appears to be 
involuntary. With the development of the disease, paresis occurs 
and stupor becomes deeper. In some cases in this stage a viscid 
secretion flows from the nostrils and mouth or the material may be 
squeezed from the nostrils. A diphtheritic type has been observed, 
in which fibrinous exudate occurs in the nasal, oral and phar\Tigeal 
cavities. Conjunctivitis and lachrymation may occur. 

As a rule there is no diarrhea. The feces are quite solid, often 
green in color and of the usual amount. In the later stages of the 
disease some birds discharge hardly any feces. At death and after, 
a fluid is discharg(>d from the cloaca and beak. 

Morbid anatomy. Freese has conducted numerous autopsies 



84 DISEASES OF DOMESTICATED BIKDS 

of naturally infected birds and describes the lesions as follows: 

Hemorrhages in the mucous membrane of the passage between the 
proventriculus and gizzard are highly characteristic of the disease. 
They also occur in the mucosa of the true proventriculus between 
the conical elevations or very seldom they are limited only to these 
elevations. It is possible for the hemorrhages to occur in both 
places in the same fowl. The hemorrhages of the mucosa between 
the papillse or in the opening between the two stomachs may be 
superficial, in the mucosa or in the tissues lying beneath. They 
vary gTeatly in size and may be barely visible or several centimeters 
in diameter. They are red or dark red in color and often are not 
sharply circumscribed. If the conical papillae are involved, either 
the whole mass is reddened or only the upper border about the 
mouth of the gland. The hemorrhages in the proventriculus in 
many cases are very small and are often quite separated, so that 
their presence might not be obsei'\'ed on superficial examination. 
This is all the more likely unless the viscid, gTay, white, cloudy 
mucus is removed. 

Small hemorrhages are frequently found in the fatty tissue sur- 
rounding the gizzard, on the mesentery of the small intestine and 
superficially under the cuticle of the gizzard. More rarely, fine 
subepicardial hemorrhages are observed in the pericardium, espe- 
cially in the heart fat, and in the tracheal, laryngeal and pharyngeal 
mucosae. They are rarely found in the pulmonary pleurge. 

The kidneys are swollen to an extraordinary extent. They are 
either grayish brown in color and clouded or in the acute cases, 
dark brown on account of the presence of an excessive amount of 
blood. 

In the functional ovary, there is a marked congestion of the 
vessels of the yolk capsules. Occasionally hemorrhages are ob- 
served under the serosa in the yolk mass. 

In acute cases a certain degree of swelling of the spleen is ob- 
served. As a rule, however, lesions of this organ do not occur. 
The liver does not show important lesions, but some writers describe 
congestion in acute cases. 

Inflammation of the small intestine is at the most limited to the 
first portion of its length. In some cases there is observed only a 
slight catarrhal inflammation, while in other cases there is a marked 
inflammation with hemorrhages. The ceca and the remaining large 
intestine are very rarely inflamed. Inflammation of the intestine 
occurs in about half of the cases. 



FOWL PLAGUE 85 

Exudate in the abdominal cavity is either serous or sero-fibrinous. 
The fibrin as a rule is in suspension in the serous fluid in the form 
of flakes, or is deposited loose on the peritoneum in the form of 
threads or sheets. 

The peritoneum is not inflamed but is smooth, shiny and trans- 
parent. Exudate occurs in the abdominal cavity in about a quarter 
of the cases. 

Exudate occurs in the pericardium in the form of a serous or 
sero-fibrinous fluid, which on opening of the pericardial sac often 
coagulates into a gelatinous mass. The presence of exudate in the 
pericardium occurs somewhat less often than in the. abdominal 
cavity. 

A bluish red coloration of the comb occurs very often. There 
is nothing characteristic about it as compared with a number of 
other diseases. 

Some authors emphasize the significance of catarrh of the upper 
air passages and of the phar^oix. They note the occurrence of 
viscid gTay white mucus in the beak, throat and nasal cavity, but it 
is considered to be a normal secretion which remains in its place 
of production for some time before death. 

In wild ducks dying of the nervous type it has been noted that 
autopsy reveals no characteristic gross changes. 

Diagnosis. The presence of hemorrhages in the proventriculus, 
the swelling of the kidneys and the severe injection of the blood 
vessels in the yolk capsules of the ovary, occasionally associated with 
the presence of hemorrhages, in birds dying of a pest-like disease, 
are most significant. The autopsy findings alone will not always 
suffice for making a diagnosis. In some cases as in other infectious 
diseases, the lesions may be so slight as not to warrant drawing 
conclusions. A diagnosis of fowl plague can be established most 
certainly by successful transmission to a hen with absence of a 
causative agent recogTiizable in tissues or in cultures from the blood 
and organs. 

Differential diagnosis. Phosphorus poisoning causes lesions 
having the greatest similarity to those of fowl pest and also causes 
a high mortality. In general the hemorrhages in the proventriculus 
occurring in phosphorus poisoning extend deeper than in fowl pest, 
also in the poisoning, erosions occur in the hemorrhagic mucosa. 
In phosphorus poisoning there is also a marked inflammation of the 
upper part of the intestine. N'otwithstanding the great similarity 
of the lesions the two conditions can be diftcrentiated at autopsy by 



86 DISEASES OF DOMESTICATED BIRDS 

the escape of the so-called phosphorus vapor from an opening in the 
gizzard or crop and by the characteristic smell. 

ISText in similarity is fowl cholera. This is characterized by the 
occurrence of subepicardial hemorrhages, an exudate in the peri- 
cardium, a marked inflammation of the intestine and by the in- 
flammation frequently occurring in the lungs. In only a few cases 
would these lesions be confounded with those of fowl pest. 

Rabbit inoculation is valuable, for this animal is immune to 
fowl pest and susceptible to fowl cholera. Spirochetosis will be 
suggested by the drowsiness and paralytic symptoms and must be 
difterentiated by microscopic examination of blood taken during an 
early stage. In spirochetosis such blood will be found to contain 
spirochetes, but such an examination will be misleading, if the 
sample be dra\\Ti after the crisis has occurred. 

Preventive measures. Treatment is unavailing. The general 
sanitary measures such as recommended for cholera, should be em- 
ployed. 

Attempts to immunize by vaccination with diluted red corpuscles 
have failed. A slight measure of success by vaccination with virus 
killed by ether, has been obtained. Birds after two vaccinations 
were protected to a slight extent in that death was delayed. 

The agency of poultry exhibitions in rapidly disseminating the 
infection should be borne in mind. The disease apparently gained 
a wide distribution in Germany as a result of a show held in Bruns- 
wick in 1901. 

REFERENCES 

1. Belfanti and Ascoli. Spigolature nella Peste Aviaria e nell' Afta. 
Clin. Vet., Vol. 39, 1916, p. 577. 

2. Centanni. Die Vogelpest; Beitrag zu dem durch Kerzen filtrirbaren 
Virus. Centralhl. f. BaUeriol. {Etc.), 1 Alt. Orig., Bd. 31, 1902, S. 145. 

3. Cominotti. Peste aviaria nella anitre. Clin. Vet., Vol. 39, 1916, 
p. 129. 

4. Dubois. Une maladie infectiense des poules a microbes invisibles. 
Compt. rend. Soc. de hiol. Vol. 54, 1902, p. 1162. 

5. Freese. Ueber Hlihnerpest mit besonderer Beriicksichtung der 
pathologischen Anatomie. Deutsche tier'drztl. Wchenschr., Bd. 16, 1908, 
S. 173. 

6. Hertel. Ueber Geflug(!l-cholera imd Hiihnerpest. Arb. a. d. Tc. 
Gsndhtsamte., Bd. 20, 1904. S. 453. 

7. Joest. Beitrag zur Kenntnis der Bakterienflora des Hiihnerdarmes 
nebst einigen Bermerkungen iiber eine neue Huhnerseuche. Berl. 
tierdrztl. ^Ycllnschr., 1902, S. 241. 



FOWL PLAGUE 87 

8. Kleine und Moellers. Ueber Hiihnerpest bei Gansen. Centralhl. f. 
BahterioL, Bd. 39, 1905, S. 545. 

9. Ivraus iind Schiffmann. Studien liber Immunisierung gegen das 
Virus der Hiihnerpest. Centralhl. f. Bahteriol. {Etc.), 1. Abt. Orig., Bd. 
43, 1907, S. 825. 

10. Landsteiner u. Berliner. Ueber die Kultivierung des Virus der 
Hiihnerpest. CeniraJhl. f. Bahteriol. {Etc.), 1 AM. Orig., Bd. 67, 1912, 
S. 1G5. 

11. Leclainche. La Peste Aviaire. Revue Gen. de. Med. Vet., T. 3, 
1904, p. 49. 

12. Lijisehiitz. L'eber mikroskopisch sichtbare filtierbare Virusarten. 
Centralhl. f. BaUeriol., Bd. 48, S. 77. 

13. Lode und Gruber. Bakteriologische Studien iiber die Aetiologie 
einer epidemischen Erkrankungen der Hiihner in Tirol. Centralhl. f. Bah- 
teriol. (Etc.), 1 Alt., Orig., Bd. 30, 1901, S. 593. 

14. Maggiora und Valenti. Ueber eine Seuche von exudativen Tyi^hus 
bei Hiihnern. Zeit. f. Hyg., Bd. 42, 1903, S. 185. 

15. Mane. Immunizierungsversuche bei Hiihnerpest. Arh. a. d. h. 
Gsndhtsamte, Bd. 21, 1904, S. 537. 

16. Ostertag und Bugge. "Weitere Untersuchungen iiber die Hiihner- 
pest. Zeitschr. f. Infehtionshr. d. Hanstiere, Bd. 2, 1906, S. 1. 

17. Ostertag und Wolffhiigel. Untersuchungen iiber die " Hiihnerpest," 
die neue Geflugelseuche. Monatschr. f. praht. Tierh., Bd. 14, 1903, S. 49. 

18. Ottolenghi. Ueber einen besonderen Befund bei der Gefliigelpest. 
Centralhl. f. Bahteriol. {Etc.), 1 Aht. Orig., Bd. 67, S. 510. 

19. Buss. Beobaehtungen iiber das Virus der Hiihnerpest. Airh. f. 
Hyg., Bd. 59, 1906, S. 286. 



CHAPTER VIII 

AVIAN TUBERCULOSIS 

Characterization. Avian tuberculosis constitutes an affection 
closely related to the same disease in mammals, characterized by the 
development of tubercles principally in the visceral organs. 

Poultr^anen refer to the disease as spotted liver, liver complaint, 
rheumatism, or describe the birds as going light. 

Species affected. A considerable number of domesticated and 
wild birds are affected. The disease has been observed in the 
fowl, guinea-fowl, peafowl, turkey, duck, goose, swan, pigeon, os- 
trich, parrot, canary, pheasant, sparrow, and in a large number of 
species of wild birds kept in zoological gardens. 

Etiology. Typical strains of the avian variety of B. tuhercu- 
losis possess characteristics enabling them to be differentiated from 
the human and bovine varieties. Avian bacilli are more readily 
isolated and cultivated in pure culture, than are the mammalian 
varieties. The avian organisms are somewhat shorter and stain 
more evenly than those of the mammalian variety. While the 
guinea pig is most susceptible to mammalian strains, inoculation 
with avian material may result in emaciation with no visible lesions, 
or in relatively slight lesions of a non-progressive character. When 
lesions are not visible after inoculation, it does not preclude the 
possibility that tubercle bacilli may be present and demonstrable 
microscopically, or culturally, or by further inoculation of the tis- 
sue into other guinea pigs. 

The transmissibility of avian tuberculosis to mammals and vice 
versa is of interest in connection with the control of the disease. 
As a general rule, fowls are not susceptible to the human and bo- 
vine varieties. Experimental evidence exists to show that calves 
may be infected by injections of avian tubercle bacilli, and that 
fowls have been artificially infected with tubercle bacilli of mam- 
malian origin. The majority of experiments to test this trans- 
mission have given negative results. In view of these findings, 
the simultaneous occurrence of tuberculosis in cattle or man, and 
in fowls exposed to infection from them, has slight value as evi- 
dence of transmission. All three varieties of the disease are so 

88 



AVIAN TUBERCULOSIS 89 

common that coincidences may occur. The literature of tuber- 
culosis reveals comparatively few instances in which avian tubercle 
bacilli have been found naturally in cattle or in man. 

"With the exception of the intertransmissibility of avian tuber- 
culosis between pigs and fowls, the disease in fowls stands by itself 
as an economic and hygienic problem. There is considerable evi- 
dence that parrots and canaries may be infected from a mammalian 
source. 

While pigs undoubtedly contract tuberculosis most frequently 
from bovine sources, they do to a lesser extent acquire it from avian 
sources. The possibility of the transmission of tuberculosis between 
pigs and fowls should not be overlooked in connection with hygienic 
measures against the disease in either. Outbreaks of avian tuber- 
culosis in pigs in contact with infected fowls have been observed 
both in Denmark and in the United States. Eastwood and Grif- 
fith made cultures from a series of seventy-eight pigs exhibiting 
only localized tuberculosis. The avian tubercle bacillus was found 
alone in twenty-six of these pigs, or thirty-four per cent. Of the 
remainder, the avian organism was found to be present along with 
bovine bacilli in two cases. 

Symptoms. Until the disease has developed sufficiently to cause 
emaciation, there are no characteristic s;)Tiiptoms, except in the rare 
cases when the skin or joints are involved. In the latter case poul- 
trymen describe the condition as rheumatism. This term as applied 
to a disease in birds is practically synon^^nous with arthritis. An- 
emia and emaciation are constant in advanced cases, the latter be- 
coming extremely marked. The loss of weight is very noticeable ; 
the bird becomes weak and moves about very little. This disin- 
clination to move may be due either to extreme weakness or, more 
rarely, to involvement of the joints. Under such conditions, the 
bird spends much of the time in a crouching position. An unnatural 
character of the gait is noticeable. 

The eyes are bright and appetite remains markedly good in ad- 
vanced cases. The skin and visible mucosae are pale, and the 
feathers are ruffled. The temperature is usually within the normal 
range, and rarely is subnormal. Young birds affected with the dis- 
ease enough to show symptoms are not encountered, doubtless due 
to the time necessary for tlie development of serious lesions. 

The separation of deaths from one another in point of time is a 
characteristic feature of the disease. 

Morbid anatomy. Emaciation is striking in most cases that 



90 DISEASES OF DOMESTICATED BIEDS 

die of the disease. The muscles of the breast may be represented by 
barely a trace. 

Avian tubercles do not differ greatly in gross appearance from 
those of the mammalian type. The smallest ones consist of nodules 
of tissue in which central caseation has not yet begun. In larger 
ones varying degree of caseation is illustrated, but calcification 
is not frequently observed. Avian tuberculosis differs from mam- 
malian tuberculosis markedly in that the visceral organs primarily 
are involved and lesions of Ijaiiph nodes are of subordinate im- 
portance. 

The liver is usually studded throughout with nodules which are 
easily separated from the hepatic tissue. There may be several sizes 
of nodules, suggesting that several corresponding invasions of bac- 
teria have occurred. The smaller tubercles are white or grayish 
white, while the larger, older ones are more yellow in color. The 
presence of the tubercles brings about secondary degenerative 
changes in the liver, as a result of which the tissue becomes pale and 
friable. As a consequence, fatal hemorrhages may occur. The or- 
gan is enlarged in advanced cases, and in exceptional cases may con- 
stitute one-fourth of the weight of the bird. 

The spleen, like the liver, is found involved in practically all 
advanced cases. The relative enlargement is greater, for this organ 
may attain the size of a walnut. The small amount of functional 
tissue remaining is often striking. 

The smallest tubercles of the intestine are located in the deeper 
layers of the mucous membrane. Slightly larger ones are in inti- 
mate contact with the intestinal wall but project somewhat. Still 
larger ones, as much as an inch in diameter, are pedunculated and 
in most cases the interior of such tubercles communicates with the 
lumen of the intestine. Lesions of the intestine also occur in the 
form of numerous but isolated ulcers on the mucous membrane. 

The kidneys, ovary, mesentery, and lungs are involved less often, 
while cases of tuberculosis of the pancreas, gizzard, and skin are 
rare in fowls. In the kidneys, the tubercles are discrete, hard, and 
glassy. These organs alone may be affected. Small tubercles are 
observed on the mesentery associated with tubercles on the intestine. 
Involvement of the lung apparently is associated Avith advanced de- 
velopment of the disease and then it occurs comparatively rarely. 
The tubercles may be isolated or aggregated into extensive areas. 
Skin lesions may consist of single spherical masses, each surround- 
ing the root of a feather, or more often, consist of larger masses. 



AVIAN TUBERCULOSIS 91 

A form of nodular disease of the skin lias been observed in which 
tubercle-like organisms are found, and efforts to cultivate them give 
negative results. Another point of difference is that the organisms 
are decolorized by acidulated alcohol, which does not occur in the 
case of true avian tubercle bacilli. Unquestionable tuberculous le- 
sions of the skin occur in pigeons. A tuberculous lesion consisting 
of a cutaneous horn is relatively common in parrots. 

Bone lesions have been observed particularly on the breast bone 
and ribs. Lesions occur in the knee, back, digital and shoulder 
joints. The extremities of the bones enlarge with accumulation of 
cheesy material, or may discharge a semi-fluid substance. 

Differential diagnosis. A diagnosis of tuberculosis by physical 
examination of the living bird is hardly possible in most cases, nor 
is this important. Emaciation creates a strong presumption of the 
existence of tuberculosis but is not conclusive, for it occurs in as- 
thenia, in serious infestation with air sac mites and in other condi- 
tions less well understood. 

At autopsy of fowls, the possibility of the occurrence of tumors 
of the liver, and nodular tseniasis of the intestines should be borne 
in mind. ^Nodular lesions not involving the liver and spleen, may 
quite safely be considered as not tuberculosis. In the turkey the 
more highly colored areas occurring in infectious entero hepatitis 
are not likely to mislead one familiar with these lesions. Gouty 
arthritis and bumblefoot in the fowl are suggestive of tuberculosis. 
JSTodules in the lung caused by aspergillosis may be differentiated 
from tuberculosis by microscopic examination. 

Microscopic examination of smears for tubercle bacilli is available 
as a means of diagnosis, especially since organisms are unusually 
abundant in lesions of avian tuberculosis. 

Tuberculin test. ISTumerous efforts have been made to apply 
the subcutaneous tuberculin test to fowls, using tuberculin prepared 
from both avian and mammalian cultures, but without success. 

Better results have attended trials with the intradermal (intra- 
cutaneous) form of the test in manner similar to that in which it 
is applied to cattle. The wattle is chosen as the site of injection 
and a very fine needle of 'No. 26 or 27 gauge is employed. The aim 
is to deposit the tuberculin not in the deeper layers, but in the 
stratum Malpighii. It should not be injected so superficially that 
the tuberculin will be lost by rupture of the epithelium. 

The tuberculin employed is prepared in the usual manner from 
an avian tubercle culture, and is diluted fifty per cent for use. The 



92 DISEASES OF DOMESTICATED BIRDS 

dose varies from one-twentieth to one-tliirtietli of a cubic centimeter. 
After short experience, attention to the graduations on the syringe 
will be abandoned and the dose judged by the appearance of the tis- 
sues at the point of injection. The head of the fowl should be held 
with considerable firmness by an assistant during the injection, in 
order to obviate the. necessity for inflicting unnecessary damage to 
the tissues, which would interfere with observing the results. Care 
must be taken to avoid injury of the wattle by rough handling. 

A positive reaction to the test consists of a swelling of the in- 
jected wattle. Perhaps ten per cent of the swellings will be so 
slight as to be doubtful. Observations made by Van Es and Schalk 
indicate that among the reactions considered by them as doubtful, 
about one-half were found on slaughter, to contain lesions, and half 
to be free from lesions. The majority of reactions will leave no 
doubt as to the existence of a pronounced edematous swelling, which 
may increase the thickness of the wattle to several times normal. 

Of 90 birds tested by Van Es and Schalk, showing typical" reac- 
tions, 88 were found tuberculous at slaughter and 2 showed no vis- 
ible lesions. Of 130 birds slaughtered and found without lesions, 
120 or 91.5 per cent had failed to react to the test. About 8.5 per 
cent of the non-reacting fowls were found to have lesions. Thus the 
results shown indicate that the intradermal tuberculin test for fowls 
is about as accurate as the same test or the subcutaneous test in 
cattle. 

The test surely furnishes information regarding the extent to 
which infection has spread in a flock and consequently provides in- 
formation regarding which birds should be eliminated. Of three 
and four year old birds in an infected flock, as high as 86 per cent 
may react. Of two year olds, 2-1 per cent and of pullets, 3 per 
cent have reacted. It may further be of use in determining whether 
or not tuberculosis exists in a flock from which it is contemplated 
to purchase birds. 

Transmission. The tendencv of lesions involving the intestine 
to perforate the wall and discharge into the lumen, provides the 
main channel for the dissemination of tubercle bacilli. Microscopic 
examination of such lesions reveals enormous numbers of the or- 
ganisms. In view of the rarity of pulmonary lesions and the rela- 
tive frequency with which intestinal lesions occur, the feces must be 
regarded as the chief channel of elimination of infection. Tubercle 
bacilli have been demonstrated to be present in the feces of infected 



AVIAN TUBERCULOSIS 93 

birds but are not found in the feces of a very large percentage of 
such birds. 

Tubercle bacilli have been demonstrated in eggs laid bv tubercu- 
lous hens but it has not been demonstrated that such a channel of 
dissemination of the infection is an important one. It seems quite 
certain that the disease is not observed in young birds as might be 
expected if transmission through the egg were common. 

Tubercle bacilli, when directly exposed, are sensitive to sunlight, 
but the conditions about poultry establishments are such as to war- 
rant belief that they may persist alive for months. 

Feeding experiments leave no doubt but that the alimentary tract 
is the chief portal for entrance of infective material. Exposure of 
healthy birds by contact with infected birds sets up disease Avhich 
may persist for a year before important lesions develop. The eat- 
ino- of carcasses of birds dead of the disease undoubtedlv contributes 
to dissemination of infection. In some cases, exposure by feeding 
infected droppings has induced disease that was fatal in six months. 

Wliile the introduction of tuberculous fowls must be regarded as 
the most common means of infecting a flock, there exists the possi- 
bility of its being accomplished by infected pigeons, among which 
the disease is not uncommon, or by pigs. 

Economic importance. Tuberculosis is capable under favor- 
able conditions of causing a very heavy death rate during the course 
of a year. Comparatively few accurate observations have been 
made in this country, but annual losses up to nearly 50 per cent 
have been reported. 

Enough reports are available from the northern half of the United 
States, the Pacific Coast, and Canada to indicate that the disease 
is prevalent in the area mentioned. 

The insidious nature of the disease contributes to the unconcern 
of the owner of an infected flock. Deaths will not occur until the 
flock has been extensively infected and when they occur, are so 
scattered in point of time that they do not cause the same concern 
on the part of the owner as would be occasioned by the same num- 
ber occurring in a short time. Consequently there is lack of in- 
centive to take up repressive measures. 

Prevention. The problem of the control of tuberculosis in 
fowls presents several features that render it much simpler than 
the corresponding problem in cattle. The productive usefulness of 
hens is ended at three years of age, when it is the common practice 



94 DISEASES OF DOMESTICATED BIEDS 

to market the birds for table use, if this indeed is not done after 
two years. Thus total replacement of stock is possible in a short 
period. The extensive use of incubators and brooders assures the 
isolation of the young from infected old birds. Where the business 
is conducted on an intensive scale on a small area, isolation of birds 
of various ages is quite often practiced. Thus ideal conditions for 
combating the disease already exist in certain plants, if indeed the 
disease does ever make considerable progress under such conditions. 
It is undoubtedly true that the disease only becomes serious v^hen 
there is unlimited opportunity for mingling of birds of various ages 
as exists where poultry are kept without restraint. This is the con- 
dition in the average small poultry yard, or in an extensive poultry 
business where the system of using unfenced colonies is practiced. 

In attempting to control the disease among unfenced birds, the 
end sought is to secure isolation of young birds and maintain it 
throughout life. 

In every extensively infected flock there will be a certain number 
of badly diseased, worthless birds, which may be recognized by 
physical means, and destroyed. The intradermal test may be ap- 
plied to determine the extent of the infection. The results of this 
test, the age of the birds and egg yield, will aid in reaching a de- 
cision as to whether all or part should be marketed at once. Many 
reacting birds will be found at autopsy, to contain very minute 
lesions and there should be no prejudice against killing such for 
food. 

Appropriate disinfection of contaminated buildings, and tempo- 
rary abandonment of areas of soil too large to disinfect, will natur- 
ally suggest themselves. 

Van Es reports upon results of testing a flock of 249 birds, of 
which 43.37 per cent were tuberculous. All reacting and undesir- 
able birds were eliminated, leaving 56 non-reacting birds. These, 
together with 47 birds purchased after the test, increased the next 
year to 249. One bird died of tuberculosis after the first test and 
had undoubtedly failed to react on account of severe lesions. A 
second test made a year after the first one revealed 2.41 per cent of 
reactors. These were regarded as having contracted the disease 
from the one non-reactor of the first test. 

Mention of hygienic measures such as good ventilation, sunlight, 
and warm quarters has no place in a discussion of the control of 
tuberculosis in fowls. The disease is a veritable scourge in parts 
of California where such hygienic conditions are most favorable. 



AVIAN TUBERCULOSIS 95 

Wild birds. Deaths from tuberculosis are frequent among wild 
birds kept in captivity. Out of 459 birds dying in the Berlin 
Zoological Gardens during a given period, 118 or 25.7 per cent were 
tuberculous. The disease was present in specimens belonging to 
10 of the 15 orders of birds represented. The other five orders were 
represented by few specimens, and the observers, Koch and Rabin- 
owitsch, believe that all orders of birds are susceptible. A similar 
examination of 500 birds from the London Zoological Garden re- 
vealed tuberculosis in 30 per cent of the birds dying. 

REFERENCES 

1. Hastings and Halpin. Avian tuberculosis. Univ. of Wis. Ag7: Exp. 
Sta. Research Bull. 28, 1913. 

2. Moore. The morbid anatomy and etiology of avian tubercvdosis. 
J. Med. Research, n. s. Vol. 6, 1904, p. 521. 

3. Van Es and Schalk. Avian tubercvdosis. North Dal-ota Agr. Exp. 
Sta. Bull. 108. 

4. Ward. Tuberculosis in fowls. Univ. of Cal. Agr. Exp. Sta. Bull. 
161, 1904. 



CHAPTEE IX 

AVIAN DIPHTHERIA AND BIRD POX 

General discussion. The group of pathological conditions re- 
ferred to by various authors under such designations as simple ca- 
tarrh, colds, contagious catarrh, influenza, coryza, roup, canker, 
diphtheria and bird pox present a complicated subject for discussion. 

The pathological features presented by the lesions of the mucosa 
of the fowl's head in the conditions described as roup or diphtheria, 
have been concisely summarized by Moore. He studied the disease 
in the eastern United States and has described three stages or va- 
rieties of lesions as follows : 

" (1) An exudate of a serous or muco-purulent character in the con- 
junctiva or nasal cavities. Ordinarily this condition cannot be recognized 
in the mouth. The mucosa in these cases is apparently but slightly 
altered. 

" (2) The mucosa over a small or larger area is covered with a spreading 
exudate of a grayish or yellow color. It is firmly attached to the mucous 
membrane and when removed leaves a raw, bleeding surface. Sections 
through this exudate and the subadjacent tissues show that the epithelial 
layer is destroyed, and the underlying tissue infiltrated with cells. The 
extent of the infiltration varies in different individuals. 

" (3) The mucosa is covered with a thick mass of exudate, varying in 
color from, a milky white to a lemon yellow or brown. It is easily re- 
moved, leaving a more or less granular and healed surface. This sloughed 
mass is frequently dried at its margins to the adjacent tissue. It emits 
a strong putrid odor, due to decomposition. The drying of the margins 
prevents the fowl from expelling the exudate after it becomes separated 
from the underlying tissue." 

In the far West and South, the lesions described will commonly 
be found accompanied by the tumor-like lesions known as chicken 
pox or epithelioma contagiosum. 

The earlier studies of the etiology of the diphtheritic lesions of 
fowls extending over a long period have resulted in a mass of con- 
clusions, in the main contradictory and confusing. Various authors 
have ascribed the lesions as due to gregarina, chlamdyozoa, coccidia 
and numerous species of bacteria. 

The discovery that the filterable virus of chicken pox is capable 

of causing diphtheritic lesions has now received abundant confirma- 

96 



AVIAN DIPHTHERIA AND BIRD POX 97 

tion and furnishes a basis for clearing up the confusion. Among 
writers who have studied both avian diphtheria and pox and who 
agree on this point are Uhlenhuth and Manteufel, Schmid, Bertegh, 
and Sigwart. 

Whether there are other specific infectious diseases of fowls char- 
acterized by diphtheritic lesions not due to pox virus, remains to be 
determined by further investigation. The idea has been advanced 
that diphtheritic lesions of the mucosa of the head of the fowl may 
result from invasion by various bacteria. 

There is gTOund for questioning the validity of differentiating 
into separate disease entities such conditions as simple catarrh, com- 
mon colds, contagious catarrh, influenza and coryza. In large in- 
fected flocks, birds with catarrhal lesions alone, diphtheritic lesions 
alone, and pox lesions alone will be found in close association with 
others perhaps exhibiting all these lesions. Clinical evidence in 
such flocks points very strongly to the conclusion that the cases 
characterized by the presence of serous exudate in the nostrils are 
but the early stages of avian diphtheria. Insufficient etiological ev- 
idence is available to justify recognizing such conditions as specific 
infectious diseases. 

Characterization. Avian diphtheria is an infectious disease, 
manifested by the formation of catarrhal exudate in the nasal cavity, 
eyes, and sinuses associated with pseudo-membranes in the mouth 
and wart-like nodules on the external surface of the head. Until 
recent years, the term diphtheria or roup was applied to cases 
showing the internal exudative lesions, while those with external 
growths were designated bird pox, chicken pox or epithelioma con- 
tagiosum. The discovery that a single causative agent can produce 
both types has resulted in the two conditions being classed as simply 
external and internal lesions of one disease. 

Etiology. Diphtheria and bird pox are caused by a virus the 
nature of which is not well known. The organism has not been cer- 
tainly identified microscopically and is so small that it will pass 
through a Berkefcld filter. However, according to Marx and 
Sticker, it will not pass through a porcelain filter. 

Widely diverging opinions concerning the nature of the virus 
have been expressed by the various writers who have studied the dis- 
ease. Friedberger and Frohner assigned protozoa of the class gre- 
garina as the cause. Borrel described certain cell inclusions for 
which Lipschiitz has suggested the name StrongyJo plasma avium. 
Halasi believes the etiological agent to be a chlamydozoon. 



98 DISEASES OF DOMESTICATED BIEDS 

Tenacity of virus. Burnet observes that finely powdered virus 
in physiological salt solution placed in sealed ampoules in a water 
bath at 60° C. is killed in about 8 minutes. At 56° C. the finely 
powdered virus does not resist longer than half an hour. In sus- 
pension in water at 37° C. it has been found inactive after 8 days; 
active after 3 days; active after 30 days at 22° C. ; active after 6 
days at 25° C. Marx and Sticker found virus active after 3 hours 
at 60° C, but the material probably was not as finely powdered as 
in the experiment conducted by Burnett. The same authors found 
that desiccated virus in ampoules deprived of air remained active 
after an hour at 100° C. Scabs exposed to the sunlight in a Petri 
dish were still virulent after two months. Reischauer observes that 
the virus resists dry heat at 80° C. for 15 to 30 minutes and moist 
heat 5 minutes at 100° C. Marx and Sticker found a suspension of 
crusts virulent after 1^ hours in a 1 per cent solution of carbolic 
acid. In solutions of 2 and 2^/2 per cent it lost its virulence. 
Reischauer notes that the virus is killed in 5 minutes by 1 per cent 
solution of potash, acetic acid or carbolic acid. Burnett kept a sus- 
pension of virus in ordinary water in a refrigerator at 6° C. for 60 
days and found it virulent after that length of time. Finely pow- 
dered virus mixed with glycerine was found to be virulent after 120 
days. 

Haring and Kofoid tested the effect of various germicides upon 
powdered pox virus. The virus was saturated with the germicide 
and after the lapse of a certain amount of time, the virus was in- 
oculated into a fowl by scarification. Five per cent carbolic acid 
failed to kill in 20 minutes ; 2 per cent liquor cresolis compositus 
failed to kill in 20 minutes ; 2 per cent potassium permanganate 
failed to kill in 20 minutes ; 2 per cent copper sulphate failed to kill 
in 20 minutes ; tincture of iodine failed to kill in 10 minutes ; mer- 
curic chloride in 1 : 1000 solution failed to kill in 20 minutes; steam 
heat at 100° C. failed to kill the virus in 5 minutes but did do so in 
30 minutes; dry heat at 200° C. killed the virus in 30 minutes. 
Powdered pox scabs saturated with physiologic salt solution and al- 
lowed to decompose for 10 days in a warm place proved non-virulent. 
Dry powdered pox scabs kept in a test tube from May, 1906, to Sep- 
tember, 1911, proved virulent. 

Pathogenicity. Diphtheria and pox are especially prevalent 
in chickens and pigeons, and are also common in turkeys, geese, 
ducks and guinea-fowl. Pheasants, quail and various wild birds are 
susceptible. 



AVIAN DIPHTHERIA AND BIRD POX 99 

Natural infection. ^Natural infection occurs under conditions 
which are not yet well understood. Apparently, the virus pene- 
trates through a slight lesion of the skin or mucous membranes and 
reaches the skin or the mucous membranes of the mouth by way of 
the blood stream. Infection by ingestion probably occurs. An in- 
stance of infection by a biting fly, Stomoxysis calritrans, has been 
reported. 

Experimental transmission. The infection may be readily 
passed from the infected to susceptible birds by rubbing infective 
material into the skin or mucous membrane of the latter, especially 
if the parts be slightly scarified. 

In the pigeon the disease occurs on feathered portions of the body. 
To secure infection it is only necessary to pull out the feathers and 
rub in the virus lightly. After five or six days the skin shows a 
characteristic swelling. The follicles are greatly enlarged and upon 
pressure, whitish plugs are forced out. 

The virus is readily transmitted from the pigeon to the fowl but 
is transmitted from the fowl to the pigeon with great difiiculty, if at 
all. Passage through the fowl appears to lower the virulence of the 
virus for the pigeon. 

Intravenous injection of the fowl with pox virus as a rule causes 
only diphtheritic lesions of the mucosa of the head, with no changes 
of the skin. This is true whether the virus which was injected, 
originated from the skin or the mucous membrane lesions. 

Inoculation of the comb with material from mucous membrane 
lesions does not always result in the occurrence of pox lesions. 
Some observers interpret these negative results as proving the ab- 
sence of pox virus in the diphtheritic material. Others regard the 
results as mere failures of pox virus to take. 

The virus is present in the circulating blood and internal organs 
in acute cases, as demonstrated by inoculation experiments. In 
some cases injection of liver and blood of birds affected with chronic 
lesions of the mucous membranes of the head, will reproduce the 
disease. When positive results occur, the incubation period is long 
and the cases induced are mild. In chronic cases, the virus in the 
blood appears to be weakened or lessened in amount. The virus 
from either skin or mucous membrane lesions, when filtered, will 
give positive results in most cases. Even if the material filtered is 
of high virulence, it will only produce mild cases of mucous mem- 
brane infection. 

The incubation period for both diphtheritic and pox lesions varies 



100 DISEASES OF DOMESTICATED BIEDS 

from 3 to 12 days, depending upon the virulence of the virus and 
the method of inoculation. After injection of filtered virus, the 
period varies from 6 to 15 davs. Isolated instances of incubation 
jDeriods to 25 days have been observed. 

Mortality. The fatalities occurring in an infected flock vary 
within a wide range depending upon individual circumstances. 
Under favorable conditions, the disease may not spread to more than 
10 per cent of exposed birds, with the death rate proportionately 
low, while in other cases 80 per cent of the exposed may become in- 
fected, with deaths relatively numerous, approaching in some in- 
stances 50 jDcr cent of those affected. The virulence of the virus 
is variable and constitutes the main element for consideration in 
each outbreak. The mortality depends, to a large extent, on climatic 
conditions. Fowls are more severely affected during the fall and 
winter months and it is during this period that the heaviest losses 
are encountered. 

Course of disease. Avian diphtheria may follow an extremely 
acute course, affected birds dying without showing noticeable ex- 
ternal symptoms which would attract the casual observer. In less 
acute cases the disease may be resisted for several days after symp- 
toms are apparent, the fowl finally succumbing apparently as a re- 
sult of toxemia, or of starvation due to eye affection which inhibits 
feeding. In" the milder, and especially in the more chronic cases, 
marked symptoms may persist for several weeks and finally result 
in recovery, in so far as outward appearances are indicative. 

Symptoms. The disease is manifested by three clinical forms : 
(1) a pure mucous membrane disease, (2) a pure skin disease, and 
(3) a combination of skin and mucous membrane affection. The 
disease usually first manifests itself in a discharge from the nostrils 
which soon becomes viscid and plugs the nasal passages. In some 
individuals the first evidence of disease presents itself in the eye. 
One or both eyes may show a sticky discharge that tends to gTun the 
eyelids and obstruct vision. The exudate continues to form in the 
conjunctival sac, causing a swollen appearance of the eye and as- 
suming a cheesy character. This, through pressure and the accom- 
panying inflammation, may produce panophthalmia and loss of the 
eye. The exudate in the nostrils also becomes cheesy in consistency 
and causes a pressure on the cleft palate and distortion of the bony 
structures of the adjacent parts. The affected bird early shows ex- 
treme dullness and loss of vitality. The tendency is to mope around 



AVIAN DIPIITHEKIA AND BIED POX 101 

indifferent to its mates, surroundings, or to a person's approach. 
The head feels warm to the touch and there may be a rise of tem- 
perature. Diarrhea is often present. Death may result within 
two or three days in severe outbreaks or the bird may linger for a 
week or more with progTessively increasing debility and more 
marked lesions. The head in many cases shows a pronounced swel- 
ling on one or both sides below and in front of the eye due to the 
accumulation of a cheesy mass within the suborbital sinus. Sneez- 
ing, which has been apparent in the early stages, gives way to a 
whistling or rattling in the throat. The inflammation in the nos- 
trils may spread to the mouth and pharynx, or even to the larynx 
and trachea, where exudates are formed which are principally of the 
croupous type. Breathing is entirely carried on through the mouth 
and the continual passage of air over the tongTie tends to dry the 
tip with the result that its surface becomes hard and contracted. 
This condition is commonly termed " Pip " and may occur in any 
affection which closes the nostrils, and compels breathing through 
the mouth. Death may be caused by dyspnea from the presence of 
massive accumulations in or upon the larynx, from toxins absorbed 
from the primary causative agents and secondary invading organ- 
isms, or from starvation, owing to inappetence, or the failure to dis- 
cover food in blind cases. JSTo doubt the combination of causes act- 
ing together are responsible for the heavy mortality, amounting to 
90 per cent in some instances, among young birds. Before death, 
the subject becomes emaciated, sleepy, and finally unconscious for 
a period of several hours. 

Mild cases show less marked disturbances and may go on exhibit- 
ing s_\anptoms for several weeks, finally apparently recovering their 
normal condition. Certain individuals retain the disease in a 
chronic state and serve as carriers for future outbreaks. 

Oftentimes the bird shows no external manifestations of illness. 
The comb and wattles have a deep red appearance and the hen con- 
tinues to lay. She dies quite suddenly and, on examination, the 
only lesion apparent is the formation of a false membrane on the 
border of the larynx or just inside that organ. This exudate has 
occluded the air passage and caused death by suffocation. Fre- 
quently the condition is discovered in time to save the fowl through 
the owner's attention being attracted by a peculiar noise which ac- 
companies the effort of the bird to breathe. It will be observed to 
open its mouth widely and attempt to dislodge the exudate by a spas- 
modic movement of the respiratory apparatus. The resulting ef- 



101 



DISEASES OF DOMESTICATED BIRDS 



feet may be termed a " bird cough." Prompt attention in such cases 
nearly always saves the life of the fowl. 

The disease spreads rapidly through a flock affecting a large per- 
centage of the birds and causing the death of a variable percentage 

according to the virulence 
of the virus. Young birds 
are especially susceptible, 
adults less so, and a few 
exhibit complete resist- 
ance. 

Morbid anatomy. The 
external lesions have the 
appearance of wart-like 
growths prominently raised 
from the surface of the 
skin. The size may vary 
to a considerable degree 
according to location, or 
through combination of 
several nodules. General- 
ly they have a diameter of 
Yg to ^/4 of an inch. 
These pox tumors occur 
chiefly on the unfeathered 
or lightly feathered por- 
tions of the body, and par- 
ticularly on the comb, wat- 
tles, eyelids and at the 
commissures of the beak. 
They may also be found at 

Fig. 8. Head of a Plymouth Rock cock affected times on the under surface 
with epithelioma contagiosum (bird pox). . ,• i i 

(j^lgg) of the wings, particularly 

if there has been an abrasion or bruise at this point They may be 
rarely observed around the vent. The nodules first appear as small 
w^hitish points which rapidly increase in size, reaching their maxi- 
mum size in four to six days. They form an integral part of the 
epithelium, being in reality an extrusion of enlarged epithelial cells. 
If the superficial scale of exudate is removed, the tumor will be seen 
to consist of whitish cylindrical masses arranged perpendicularly to 
the skin. The mass assumes a yellowish color which later changes 
to a dark bro^vn or black as the tuberosity degenerates and develops 




AVIAN DIPIITIIEEIA AND BIRD POX 103 

into a hard dry scab. After seven to nine days this scab may be 
easily removed leaving a whitish area only slightly elevated above 
the surface and usually pitted. The scabs retain the virus of the 
disease and Avhen rubbed on the scarified skin or mucous membrane 




Fig. 9. Head of a turkey affected with epithelioma 
contagiosum (bird pox). (Klee) 

of the mouth, even after a period of five years, may reproduce typical 
lesions. 

Haring and Kofoid describe the microscopic structure of chicken 
pox tissue as follows : 

" The epithelial tumors are produced by a hyperplasia of the epithelium 
due to an increase both in the size and number of cells. The zone of 
growth is in the stratum of Malpighii, the principal region of prolifera- 
tion being in the outer edges from which the cells increase in both direc- 
tions. A proliferating epithelium forms cell nests surrounded by thick 
bands of connective tissue, which contain blood vessels with thickened 
walls. The rapidly proliferating peripheral cells of the Malpighian layer 
are seen thickly studded with granules. The nucleus contains deeply 
staining chromatin bodies which are in an active process of proliferation. 
Ivaryokinetic figures are common in this region. More deeply in the 
epithelial tumor mass the cells are greatly increased in size and haA^e rela- 
tively fewer granules. The nuclei are nale and show little evidence of 
cell division. In these cells, are large cell inclusions which are very strik- 
ing in appearance, and which Eeischauer and others have thought to be 
protozoa. There is usually but one of these bodies in each cell. They 
vary in size from five to twenty microns, most of them are round, al- 
though some of them are quite irregular in shape. They are evidently 
fatty in structure as they stain black with osmic acid. When eosin and 
methylene blue are iised, they stain a faint pink, resembling somewhat the 
Negri bodies found in the brain tissue of rabid animals, although they are 



104 DISEASES OF DOMESTICATED BIRDS 

usually much larger. They seem to have no definite internal structure, 
being- usually homogeneous in appearance. Deeper in the epithelial mass 
the cells are very large and show evidence of degeneration, here the cyto- 
plasm stains poorly and has but few granules. Burnett has called this con- 
dition hydropic. In the center of the older epithelial cell masses, the cells 
are so degenerated that they form a necrotic mass. The nucleus, of the 
cell first degenerates. The cause of this degeneration is probably due to 
the fact that the cell nests increase in size by multiplication at the peri- 
phery. The outside cells consume all the nutriment at the expense of the 
central ones and cause their degeneration. The central necrosis rapidly 
extends, involving the greater part of the tumor mass." 

The cell inclusions characteristic of pox have been studied ex- 
tensively and the interpretation of their nature and significance has 
been the subject of much discussion. Some observers see in them, 
stages in the life of a protozoan, while others regard them as products 
of degeneration of the cell. 

In the early stage of false membrane formation, the external layer 
of the mucosa is principally involved. There is an exfoliation of 
the cells, which become swollen and amorphous. The cell proto- 
plasm early loses its identity, while the nuclei disintegrate more 
slowly and appear as independent bodies showing different degrees 
of degeneration. ]\rucous exudates which have undergone coagula- 
tion, together with the epithelial cells, enclose leucocytes in various 
stages of degeneration. An edematous area is formed around the 
membrane, and wandering leucocytes are observed in the ^Malpiiihian 
layer of the mucosa. During this stage there is a well marked line 
of differentiation between the morbid area and the comparatively 
unaffected base. As the pseudo membranes are extended, the under- 
lying tissues are more deeply involved. The deeper epithelial cells 
become infiltrated and exhibit cloudy swelling. A fibrinous exudate 
accumulates which holds the cell elements in a compact tenacious 
mass. In this may be observed numerous organisms, principally of 
the bacterial type, which are to be considered as secondary invaders. 
Protozoal organisms may also be present including flagellates, amebas, 
coccidia and other forms. Some investigators have attributed the 
origin of avian diphtheria to certain of these protozoa. However, the 
evidence brought out has not been sufficient to establish these organ- 
isms as specific causes. The course of development of filterable 
viruses in the animal system is a problem which has not been satis- 
factorily solved, and until this is accomplished, it is unsafe to give 
etiologic sigTiificance to organisms or cell inclusions which may be 
found associated with certain morbid conditions. 



AVIAN DIPHTHEEIA AND BIRD POX 105 

The gross lesions of the mucous membranes are not characteristic 
of infection with pox virus alone. Ilaring and Kofoid have pro- 
duced similar lesions by mechanical injuiy or by the injection of 
pyogenic bacteria. However, in diphtheritic lesions not due to pox 
virus, the cell inclusions characteristic of pox infection are not 
present. 

Diagnosis, In typical outbreaks, the disease is readily recog- 
nized by the closely adherent pseudo membranes on the mucosa of 
the mouth and pharynx, and by the characteristic nodules on the comb 
and wattles. When the latter are present, the diagnosis is estab- 
lished. 

Treatment. This, to a certain extent, must be individual and 
according to the stage of the disease. When the excretions are watery 
or viscid they may be partially removed from the nostrils by pressing 
on both sides with the fingers in a manner which will force the ma- 
terial through the openings. The nasal channels are then flushed out 
with an antiseptic solution such as permanganate of potash in 2 per 
cent solution, or boracic acid in 3 per cent solution. This can be ac- 
complished by means of a syringe or medicine dropper. The most 
eft'cctive method, however, is to submerge the head in the antiseptic 
solution for a period of 30 seconds, keeping the mouth open and the 
beak elevated to permit the air to escape from the nostrils and be 
replaced by the fluid. The treatment should preferably be repeated . 
twice daily. 

Certain features of the structure of the fowl's head interfere with 
natural drainage in diseased conditions, and likewise, interfere with 
medication. The sub-orbital sinuses so often involved, have no nat- 
ural drainage. The passages connecting them with the nasal cavity 
lead upward, with the result that fluids cannot escape. The tur- 
binated bones also impede the exit of tenacious exudate. The pres- 
ence of exudate in both the turbinated bones and in the sub-orbital 
sinuses prevents access of fluid to the aft'ected mucosa. 

When patches are present in the mouth, they should be carefully 
removed mechanically before treating as above ; or the aft'ected areas 
may be swabbed with tincture of iodine, 2 per cent carbolic acid, 70 
per cent alcohol or argyrol in 20 per cent solution. Swellings of the 
sides of the head are to be freely opened and the contents removed. 
The eyes should be kept free of exudate and a mild antiseptic instilled 
between the eyelids. For this purpose argyrol in 20 per cent solu- 
tion has given the best results. Two drops are placed beneath the 
eyelid twice daily. The lachrymal duct and nostrils are also bene- 



106 DISEASES OF DOMESTICATED BIRDS 

fited by the eye injection since the solution passes into them from the 
eye. In the case of severe eye involvement it may be necessary to 
feed the fowl artifically because of the difficulty encountered by the 
bird in finding its food. The question of whether it is profitable to 
treat all cases rests with the individual owner. 

Since the pox tumors disappear in the natural course of the dis- 
ease, the value of medicinal agents in hastening this end is ques- 
tioned. Among the remedies that have been recommended are tinc- 
ture of iodine, an ointment of glycerine, vaseline or lard containing 
2 per cent of carbolic acid and 70 per cent alcohol. 

Prevention. In some instances infection is brought to a flock 
by new birds from infected flocks, or by exposure at shows. It is 
possible that infection is carried on the clothing of persons who have 
been among infected birds, or by materials on w^hich the excretions 
of diseased birds have been deposited. Free flying birds may also 
serve as carriers although it is quite likely that they are rarely re- 
sponsible for outbreaks. Newly purchased fowls and those which 
have been exhibited at shows should be quarantined on their arrival 
for a period of two weeks and carefully examined before being set 
free among others. When a fowl is observed to be ill with sym]j- 
toms of diphtheria, it should be isolated immediately. Often it is 
good policy to destroy the patient because of the danger of the 
attendant who is treating the bird carrying the virus to healthy 
fowls. Those handling diseased fowls should disinfect their hands 
before feeding or caring for others. It would also be advisable to 
wear rubbers in the hospital and remove them on leaving in order 
to gTiard against carrying infection on the shoes. 

When infection has broken out in a flock particular care should 
be exercised in keeping the houses as clean as possible. They should 
be disinfected by spraying or washing with carbolic acid in 5 per 
cent solution, compound cresol in 2 per cent solution, or formaldehyde 
in 2 per cent solution. The yards may be spread with unslaked lime 
or chloride of lime, or the soil should be plowed imder. All birds 
that die should be burned or buried deep. Those which have re- 
covered, if retaining any evidence of the disease, should be destroyed, 
as certain ones may serve as carriers and furnish the source of a 
future outbreak. The drinking water may be medicated with per- 
manganate of potash. A sufficient amount of the latter should be 
employed to give the water a deep purple color. 

Immunization. An attack of the disease confers an immunity 
complete in from 12 days to 3 weeks but which varies in duration 



AVIAN DIPHTHEKIA AND BIRD POX 107 

and degree according to the severity of the infection. Thus, chronic 
mild infection of the mucous membrane does not always produce ab- 
solute immunity. Infection of the mucous membranes alone will 
induce an absolute immunity against inoculation of the skin. Vari- 
ous authors have demonstrated immunity in fowls for periods vary- 
ing from 2 months to 2 years. Live virus only has been shown to 
confer immunity and the injection of killed virus has no immunizing 
effect. 

A number of Avorkers have attempted the immunization of fowls 
against diphtheria and chicken pox and treatment of the same 
conditions by means of a vaccine prepared from the exudates and 
pox nodules of affected fowls. The material is ground up in a suf- 
ficient amount of normal salt solution to form a suspension and is 
filtered through cotton to remove large particles. It is then diluted 
until it appears moderately cloudy and heated at 55° C. for 1 hour. 
Doses of 1 c.c. are injected subcutaneously on two or three occasions 
with intervals of 5 to Y days. 

A product prepared by this method has been favorably reported 
upon as an immunizing and curative agent by several workers. Ex- 
periments by the present writers have not sustained the claims made 
for the immunizing value of a vaccine prepared by this method. 
Fowls which have been vaccinated and later artificially inoculated 
with virulent material have developed characteristic internal and ex- 
ternal lesions of diphtheria with accompanying fatalities. 

Bacteriology of avian diphtheria. Many investigations of the 
bacteriology of avian diphtheria w^ere made previous to the recogni- 
tion of the role of pox virus in causing diphtheritic lesions, so it 
is not possible to determine whether the lesions were primarily due 
to pox virus, or were due to bacteria alone. Other reports of in- 
vestigations conducted more recently do not contain evidence that 
pox virus was not concerned in the causation of the lesions. 

Extensive investigations of the bacteriology of avian diphtheria 
have been made by Harrison and Streit, Bordet and Fally and by 
Hausser. 

Moore first reported finding a member of the hemorrhagic septi- 
cemia group in diphtheritic lesions in fowls, which observation has 
been confirmed by a large number of investigators. Sig\vart has 
observed the spontaneous appearance of fowl cholera in birds af- 
fected with diphtheritic lesions of the mucous membranes. In these 
cases the primary cause of the diphtheritic lesions was considered 
to be pox virus. He explains the occurrence by assuming that the 



108 DISEASES OF DOMESTICATED BIRDS 

pox lesions favored the increase of virulence of saprophytic hem- 
orrhagic septicemia organisms commonly present in the mouth. 

Jackley has worked on the bacteriology of roup, reaching the fol- 
lowing conclusions : 

" 1. A bacterium, designated culture ' 33A,' having all of the morplio- 
logical, cultural and biochemic characters of the pasteurella group, ap- 
parently deserves recognition as the etiological factor in roup. 

" 2. The organism has been recognized by smears in all cases of roup 
examined. 

" 3. It has been isolated and grown upon artificial culture media and 
the characteristic local lesions of the disease again reproduced. 

" 4. Finally, an absolute protection has been shown against the natural 
disease after immunization with a pure culture bacterin of this organism." 

Beach, Lother and Halpin isolated from roup lesions an organism 
probably belonging to the hemorrhagic septicemia group. Injection 
of killed culture was shown to produce immunity against injection 
with virulent culture. The organism was regarded as a secondary in- 
vader, as it did not produce lesions of roup or chicken pox. It was 
regarded as of importance as a secondary invader in wound infection. 

The identity in name and similarity of lesions of diphtheria in 
man and in birds has attracted attention to the possible relationship 
between the two diseases. There is no doubt that the two diseases 
are quite distinct in etiology even though rare cases of infection of 
birds with Bacterium diphtheria? have been reported. 

SIMPLE CATARRH OR COLD 

This condition is a mild inflammation of the nasal passages and 
is common to all species of domesticated birds. It cannot be differ- 
entiated from the early stage of avian diphtheria. 

Etiology. No definite cause may be assigned to this affection. 
It has been asserted that weak or improperly nourished birds are 
more likely to be attacked than strong, vigorous, well nourished in- 
dividuals. Exposure to unfavorable conditions in which rain or 
dampness accompanied by cold draughts tend to so aifect the mucous 
membranes of the nostrils that the various organisms which are nor- 
mally present in this region become pathogenic, has been held to be 
the primary contributing cause. 

Symptoms. The aft'ected fowl is more or less dull in appearance, 
according to the severity of the attack. The appetite is diminished, 
breathing becomes difficult, and a watery discharge from one or both 
nostrils is early in evidence. This discharge may disappear in the 



AVIAN DIPHTHERIA AND BIRD POX 109 

course of two to four days, or it may take on a viscid consistency, 
closing the nasal openiniis and necessitating breathing through the 
mouth. The discharge may also escape through the mouth. This 
is rendered easy by the cleft palate peculiar to birds. 

Morbid anatomy. The mucous membrane of the nasal passages 
becomes swollen and congested and an excessive secretion of mucous 
fluid is poured out. 

Treatment. As the disease is of short duration, it is usually 
only necessary to place the patient under more favorable conditions 
to bring about recovery. In the more severe cases, the nostrils should 
be washed out twice daily with boracic acid in 3 per cent solution, or 
creolin in 1 per cent solution. 

REFERENCES 

1. Beach. Suggestions to poultrymen concerning chicken pox. Univ. 
of Calif. Coll. of Agr. Circ. No. 1^5, 1915. 

2. Beach, Lothe and Halpin. An outbreak of roup and chicken-pox in 
which the high mortality was apparently caused by a secondary invader. 
J. Agr. Research, Vol. 17, 1915, p. 554. 

3. Bertegh. Ueber die Beziehungen zwischen Geflugeldiphtherie und 
Gefiiigelpocken. Centralhl. f. Bakteriol. (Etc.), 1. AM., Grig., Bd. 67, 
1912, S. 43. 

4. Bordet and Fally. Le microbe de la diphtheric des poules. Ann. de 
r Inst. Pasteur, T. 24, 1910, p. 563. 

5. Burnet. Contribution a I'epithelioma contagieux des oiseaux. Ann. 
de v. Inst. Pasteur, T. 20, 1906, p. 742. 

6. Gallagher. Epithelioma contagiosum of quail. /. Am. Vet. Med. 
Ass., Vol. 3, 1916, p. 366. 

7. Hadley and Beach. Controlling chicken-pox, sore-head or contagious 
epithelioma by vaccination. Proc. Am. Vet. Med. Ass., 1913, p. 704. 

8. Ilalasi. Beitrage zur Kenntniss de Geflugelpocke luid der Geflugel 
diphtheric. Inaug. Diss. Kozl. 

9. Haring and Kofoid. Observations concerning the pathology of roup 
and chicken pox. P^^oc. Am. Vet. Med. Ass., 1911, p. 413. 

10. Harrison and Streit. Roup. Ontario Agr. College. Bulls. 125 and 
132. 

11. Hausser. Bacteriologische Untersuchungei) iiber Geflugeldiphtherie. 
Centralhl. f. Bahteriol. {Etc.), 1 AM. Orig., Bd. 48, 1909, S. 535. 

12. Jackley. A study of the etiology of roup in birds. Kansas Agr. 
Exp. Sta. Tech. Bull. U. 1917. 

13. Mack. Tbe etiology and morbid anatomy of diphtheria in chickens. 
Am. Vet. Bev.. Vol. 28, 1905, p. 919. 

14. Mack and Records. The control of epithelioma in chickens by vac- 
cination. Nevada Agr. Exp. Sta. Bulls. 82 and 8k. 

15. ]\''qnteufel. Beitrage zur Kenntniss der Tmmunitatserscheinungen 
I"i dert pogennannten Gefliigelpocken. Arh. a. d. k. Gsndhtsamte., Bd. 33, 
1909-10, S. 305. 



110 DISEASES OF DOMESTICATED BIRDS 

16. Marx u.' Sticker. Untersuchungen iiber das Epithelioma contag- 
iosum des Gefliigels. Deutsche Med. Woch., Bd. 28, 1902, S. 893. 

17. Moore. A preliminary investigation of diphtheria in fowls. U. 8. 
Dep. Agr. Bureau Animal Indust., Bull. No. 8, 1904. 

18. Miiller. Zur Aetiologie der Gefliigeldiphtherie. Centralhl. f. Bak- 
teriol. (Etc.) 1 Alt. Orig., Bd. 41, 1906, S. 423. 

19. Reischauer. Tiber die Pocken der Vogel, ihre Beziehungen zu den 
echten Pocken und ihren Erreger. Centralhl. f. BaMeriol. {Etc.), 1 Aht. 
Orig., Bd. 40, S. 356. 

20. Schmid. Untersuchungen iiber der Beziehungen zwischen Gefliigel- 
diphtherie und Epithelioma contagiosum. Centralhl. f. BaMeriol. {Etc.), 
1 Aht. Orig., Bd. 52, 1909, S. 200. 

21. Sig-wart. Experimentelle Beitrage zur Frage der Identitat von 
Gefliigeldiphtherie und Gefliigepocken. Cenlralhl. f. BaMeriol. {Etc.), 1 
Aht. Orig., Bd. 56, 1910, S. 428. 

22. Sweet. A study of epithelioma contagiosum of the common fowl. 
Univ. of Calif. Puhs. in Zoology, Vol. 71, 1913, p. 29. 

23. Uhlenhuth imd Manteufel. Neue Untersuchungen iiber die 
atiologischen Beziehungen zwischen Gefliigeldiphtherie (Diphtheria 
avium) und Gefliigelpocken (Epithelioma contagiosum). Arh. a. d. Jc. 
Gsndhtsamte, Bd. 23, 1909-10, S. 288. 

24. Ward. Poultry diseases in California. Proc. Am. Vet. Med. Ass., 
1904, p. 164. 

25. "Ward. Observations on roup in chickens. Proc. Am. Yet. Med. 
Ass., 1905, p. 198. 



CHAPTER X 

ASPERGILLOSIS AND FAVUS 



ASPERGILLOSIS 

Synonyms. Pneumo-mycosis, brooder pneumonia. 

Characterization. Aspergillosis is a disease of the pulmonary 
region due to infection with fungi. It is characterized by the forai- 
ation of an exudate, usually of a moldy appearance, on the mucous 
membrane of the air passages, principally the air sacs of the ab- 
dominal cavity. 

Etiology. The disease is almost invariably introduced by fungi 
of the genus Aspergillus, Aspergillus fumigatus being the most con- 
stant causative agent. Other members of the aspergillus group have 
been identified in the morbid processes. These, however, are of 
slight sigTiificance as they have not been associated with the incidence 
of pulmonary mj'cosis to any great extent. 

Aspergillus fumigatus is widely distributed in nature and is often 
observed on vegetable matter of all kinds which has been exposed 
to dampness. Birds scratching 






among moldy grains or in moldy 
litter may inhale the spores. 
These find a favorable place for 
propagation on the mucosiie of the 
bronchi, or of the air sacs. 

The fungus may be readily 
grown on potato, rye bread or 
plain agar which is acid in reac- 
tion. The most suitable temper- 
ature is between 35° and 40° C. 
The growth appears after 24- 
hours incubation as a whitish 
downy layer over the surface of 
the medium. This is composed 
of an interwoven mass of trans- 
parent mycelial threads which later give off branches capped by fruit 
heads. Each of the latter is composed of a mass of small rounded 

]ll 




FiG. 10. Aspergillus fumigatus. 
(Kedrawn from jMoliler and Buck- 
ley ) 



112 DISEASES OF DOMESTICATED BIRDS 

bodies closely associated in the form of a ball, the outer area of which 
shows radiating- lines of spores. These are clear and hig-hly refrac- 
tile. Their diameter varies from 2.5 to 3.5 microns. The color of 
the growth olianges with age, succeeding from white to greenish and 
later, in old cultures, to a bro^vnish color. The spores are quite re- 
sistant. They are not destroyed by heating at 05° C. for a period 
of seven hours and require an exposure of 12 hours to a 5 per cent 
solution of carbolic acid for their destruction. In the dried state, 
they are very resistant and may germinate after several months or 
even several years when conditions are favorable. 

Pathogenicity. Of the aspergillus group, A. fumigatus is the 
most pathogenic to birds. A. nigressens, A. glaucus and A. candidus 
are less pathogenic in the order named. 

All species of birds are apparently susceptible to infection. Do- 
mesticated ones, especially those confined in large flocks and exposed 
to moldy organic matter, are most often affected. These include 
chickens and pigeons. Young chicks frequently are attacked by an 
acute form known as brooder pneumonia. Cage birds, particularly 
those in zoological gardens, are often fatally affected. In France 
thousands of pigeons are fed by men in a manner similar to the 
method used by parent pigeons in feeding their young; viz., loading 
the mouth with grain and fluid and passing it directly to the mouth 
of the pigeon. Among these men severe cases of pulmonary aspergil- 
losis occur as a result of their exposure to contaminated gTain. 

The disease may be transmitted artificially to animals and birds 
by inoculation or by causing the organism to be inhaled. Inocula- 
tion of small quantities of spores into the veins or peritoneal cavity 
of rabbits, guinea pigs, fowls, or pigeons causes death from septi- 
cemia in from 24 hours to 1 or 2 weeks. In the older cases necrotic 
areas are present in the visceral organs and the aspergillus fungus 
is readily isolated from these. Lesions resulting from inhalation 
infection are usually confined to the air passages. Fowls and ani- 
mals exposed in rooms to dust or rye flour containing aspergillus 
spores, have contracted the disease and died as a result. 

Aspergillosis in the ostrich is discussed on pp. 228 and 229. 

Mortality. Fatalities may be high in broods of chicks that^have 
been extensively exposed to infection. Those attacked apparently 
all succumb. Older birds are quite resistant. Evidence points to 
the conclusion that once the disease is established in the system a 
fatal termination follows. 

Symptoms. Considerable variation in the external signs of as- 



ASPERGILLOSIS 113 

pergillosis may be expected. As a rule the morbid condition has 
existed for some time before symptoms are noticed. When the le- 
sions are located in the trachea or bronchi, hoarseness of breathing, 
or a rattle in the throat may be the only indication of infection in the 
early stages. In air sac involvement alone no respiratory symptoms 
are shown. It is doubtful if external symptoms of infection of the 
air channels of the bones of the wing are manifested. 

As the disease progresses the bird becomes dull and less active. 
There is a noticeable decrease in w^cight accompanied by emaciation. 
The term " going light " is frequently applied to this condition. Di- 
arrhea is not a constant symptom but is usually present in the later 
stages. Temperature elevation is not constant in the more chronic 
form. Difficult respiration, sleepiness, extreme weakness and marked 
emaciation precede death. The appetite decreases as the disease pro- 
gresses. Death results from asphyxia and toxemia. 

In baby chicks the symptoms are apparent early and are similar 
to those of bacillary white diarrhea and intestinal coccidiosis. In 
both young and old birds the lesions observed at post mortem readily 
reveal the nature of the disease. 

Morbid anatomy. The lesions are principally confined to the 
respiratory system. This system is complicated in birds for in addi- 
tion to the lungs it includes several air sacs in the peritoneal cavity 
and air channels in certain of the bones. In some instances through 
penetration of the walls of blood vessels by the mycelia, new areas 
of infection may be established in other organs as a result of meta- 
stasis. 

The mold may develop at any point on the respiratory mucous 
membrane or may be spread over a large portion of its surface. Our 
observations at numerous autopsies place the abdominal air sacs as 
the most severely involved region. The morbid process is manifested 
by the presence of a membrane of greater or less thickness depend- 
ing on its location on the mucosa, or at times by nodules in the 
parenchyma of the lungs. In the trachea and bronchi the false 
membrane is comparatively thin while in the air sacs it may be 
much thicker and give a rigid contour to these organs. Frequently 
the sacs are filled with fungoid growth and cellular exudate, the 
whole forming a solid mass. The bronchioles may also be plugged 
with mycelia, spores and cellular exudate consisting of exfoliated 
epithelial cells, leucocytes and occasionally red blood corpuscles. 
The surface of the membrane may be grayish or gTeenish in color. 
The latter color is nearly always in evidence at some point. It is in 



114 DISEASES OF DOMESTICATED BIRDS 

this area that numerous spores may be demonstrated on microscopic 
examination. 

The mycelial threads penetrate the mucosa to the submucosa or 
may enter the adjacent blood vessels forming thrombi and establishing 
an area of necrosis resulting in a nodular formation similar to that 
of tuberculosis. In the abdominal region the organs in contact with 
the air sacs are often involved through adhesions or direct passage 
of the fungus into their interior. 

In the main, the pathologic condition progresses by direct contact. 
Organs affected through the blood stream reveal small areas of ne- 
crosis in which the mycelial threads may be detected. The kidneys 
are more often affected in this manner than the liver. Artificial 
inoculation through hypodermic injection, intraperitoneally or in- 
travenously, produces extensive lesions in these organs. 

The mycelia may be demonstrated microscopically in necrotic 
areas or in nodules in the earlier stages of development. Mycelia 
may also be observed in the mucous membrane lesions, and espe- 
cially in greenish colored areas are spores readily discovered. The 
tissues surrounding the growths are found infiltrated with small 
round cells, leucocytes and connective tissue cells, indicating an at- 
tempt on the part of the system to build a protective wall against the 
spread of the parasite. This attempt is usually abortive although 
evidence of regenerative changes are apparent in some lesions. 
Giant cells are also occasionally present in the tubercle forma- 
tions. 

Course of disease. Among older birds the disease has a tend- 
ency to occur sporadically, more or less extensive intervals elapsing 
between deaths from this cause in a particular flock. Where the ex- 
posure is great, outbreaks of considerable importance may result. 
The resistance of vigorous individuals, however, is high and epi- 
zootics such as are associated with certain other diseases are rarely 
encountered. In gi-own birds aspergillosis follows a semi-acute or 
chronic course. Death may occur in from 1 to 8 weeks. In brooder 
chicks resistance is less pronounced and acute outbreaks often follow 
exposure to moldy food or material. The disease runs a rapid course 
with fatal termination in 2 to 7 days. Birds confined to limited 
areas as is the case in zoological gardens, show a high percentage 
of fatalities from this cause. 

Diagnosis. Tuberculosis, coccidiosis and aspergillosis are not 
readily differentiated sjnnptomatically in grown fowls. On autopsy 
the lesions are quite distinctive. Tuberculosis principally affects the 



ASPERGILLOSIS 115 

liver, intestine and spleen, being less of a pulmonary disease in 
birds than is the case in other animals. The tubercles are of a 
fleshy type on cross section and show small yellowish points. Coc- 
cidiosis is practically confined to the intestinal tract. Its lesions 
are of a necrotic type involving principally the duodenum and ceca. 
Aspergillosis tends to localize on the walls of the air passages and 
forms a moldy growth generally exhibiting a greenish tinge, at least 
in spots. 

Microscopic examination of the morbid material furnishes a spe- 
cific diagnosis since the causative organisms in each case are usually 
numerous and very different in morphology. 

The disease in young chicks called brooder pneumonia, shows 
symptoms similar to those of bacillary white diarrhea and cocci- 
diosis. In all three the chicks have a droopy appearance associated 
with diarrhea and loss of appetite. In general it may be said that 
bacillary white diarrhea is more highly fatal, with deaths occurring 
shortly after hatching. Coccidiosis usually appears at a later period 
and is also apt to result in heavy losses. Autopsy is necessary, how- 
ever, for positive diagnosis. The lesions in the air passages are not 
as extensive as in older fowls because of the acuteness of the af- 
fection, but may be discerned by careful examination. Bacillary 
white diarrhea is a purely septicemic disease, while coccidiosis usu- 
ally shows intestinal lesions with accumulation of necrotic or blood 
stained material in the ceca. Microscopic or cultural methods may 
be resorted to in obscure cases. 

Treatment. It is inadvisable to attempt treatment because of 
the deep seated position of the parasitic fungiTS, its resistance to 
remedial agents and the advanced stage of the attack when symptoms 
are observed. 

Prevention. The widespread distribution of Aspergillus fiimi- 
gatus renders absolute prevention difficult. Care in the selection of 
grain and litter will minimize to a great degree the chances of in- 
fection. Good housing arrangements which guard against dampness 
will prevent the propagation of molds if present to a slight extent in 
feed or litter. When the disease is discovered in a flock the source 
of infection should be located. The feed may have a musty odor or 
a greenish appearance in places, or straw litter may be moldy. In 
the former instance cooking will destroy the fungus. Moldy litter 
should be discarded. 

Experiments have shown the possibility of infection being carried 
to newly hatched chicks through the egg.. The mycelia of the fungus 



116 DISEASES OF DOMESTICATED BIRDS 

are known to be capable of penetrating the egg shell and developing 
in the albuminons material with consequent destruction of the em- 
bryo. The aspergillus colony may be observed as a dark spot on 
the internal membrane of the air chamber. Infection through this 
source is no doubt rare. It may be giiarded against by using clean 
straw or chaif in nests for laying or sitting hens, and by dipping 
eggs for hatching in grain or wood alcohol before incubating. Feed- 
ing discarded eggs to young chicks is dangerous since these may 
carry the causative organisms of several diseases. 

FAVUS 

Syno)itj]ns. White comb; favus de la poule (French); Weisser 
Kannn (German). 

Characterization. Favus is a contagious, chronic disease of the 
skin characterized by the presence of white areas most commonly 
localized on the head and is caused by a fungiis. 

Etiology. The fungiis causing the disease is designated Loplio- 
pliyton gaUi)ia\ It grows readily on agar containing 1 per cent 
peptone and 4 per cent of glucose or maltose at room temperature 
when the medium is seeded with material from the diseased patches. 
Growth first appears as a small, round, pure white, downy colony. 
As it enlarges it takes the form of a button which is slightly cup 
shaped. The culture ordinarily remains white if kept at a low 
temperature. At 27° to 37° C. the colony takes on a delicate rose 
color, becomes umbilicated, wrinkled and divided into sectors by 
lines radiating from the center. At 30° C. the culture is wholly 
rose colored, but more or less deep depending upon the culture. 
Sometimes the color varies in the same culture tube. The diffusion 
of the raspberry color in the medium is said to be an exclusive char- 
acter of the species in question. 

Pathogenicity. The infection is readily transmitted to a fowl 
by rubbing the comb with scales from a diseased bird. The disease 
is unmistakably present on the fifteenth day after inoculation and 
persists for months. Similar results are obtained with cultures. 
Mice, rabbits, guinea pigs and man are susceptible. Infection may 
occur through direct or indirect contact. 

Symptoms and morbid anatomy. The disease first appears on 
the head and its appendages such as the comb, wattles and barbs. 
ISTearly always the initial lesion is in the vicinity of the beak, in the 
form of numerous small white points. Under a magnifying glass 



ASPERGILLOSIS 



117 




they are seen to be covered with a fine, short down which later 
disappears quickly and does not return again. The white point en- 
larges and forms a layer 1 or 2 mm. thick adhering to the epidermis 
underneath. The color is generally white or gray. In time the 
thickness of the crusts increases 
as do the surface dimensions. 
Finally the small patches origi- 
nally isolated, coalesce. The ex- 
tension is regular. A white patch 
may reach the dimensions of the 
comb itself. Sometimes the di- 
mensions of a patch remain small 
but it is not rare to observe 
patches 7 or 8 cm. long and 3 or 
4 cm. broad on large combs. 

The diseased area examined 
closely presents for study thin 
places and thick places. Those 
which form small hard eminences 
of a grayish white color or slight- 
ly reddened at the top, are irregu- 
larly disseminated over the area 
of the plaque. Between these 
elevations the patch is merely a thin membrane of a pearly white 
color. Wherever the white area is thickened, the scratching detaches 
small fragments like a white powder, of which certain pieces resem- 
ble mica flakes. 

When the lesion in extending, encounters the feathers, its appear- 
ance changes slightly. A deposit of whitish crusts accumulates at 
the base of each feather. Some feathers fall out spontaneously, and 
all those which have this squamous collar at the base, have little re- 
sistance against being plucked. If a feather is pulled it comes out 
entire with its yellow root part, but it bears with it, like a collar, the 
whitish deposit which surrounds the point where the feather emerges 
from the skin. 

Course of disease. The disease is benign. Instances in which 
affected birds become cachectic and die, are exceedingly rare. Ee- 
covery may occur in three months spontaneously, or the disease may 
last for years. Long duration may be considered as an example of a 
succession of infections, rather than the persistence of one infec- 
tion. The disease persists in subjects associating with other infected 



Fig. 11. Favus, involvino; tlie head. 
(Drawn from photograph by Sabour- 
aud, Suis and Suffran) 



118 



DISEASES OF DOMESTICATED BIKDS 




Fig. 12. Deposit of crusts on quills of feathers occurring in favus involving 
feathered areas. (Drawn from photograph by Sabouraud, Suis and 
Suffran ) 

birds, in infected quarters, while there is a tendency to recovery 
when affected birds are isolated. 

Treatment. Isolation of affected birds from the flock and from 
other infected individuals in some cases is sufficient to cause the 
disappearance of the disease. Previous to the application of any 
remedy the affected areas should be softened with soap and warm 
water, after which as much of the deposit as possible should be re- 
moved. The comb lesions may be treated with carbolized vaseline 
or green soap containing five per cent of carbolic acid. A mixture 
of glycerine 6 parts and iodine 1 part has been employed on the comb 
as have salicylic acid ointment (1 : 10) ; tincture of iodine diluted 
with equal parts or more of alcohol ; five per cent formalin ointment 
or solution ; and an ointment made of red oxide of mercury 1 part, 
to 8 parts of lard. A 1—500 solution of bichloride of mercury may 
be used among the feathers. 

Prophylaxis. In an infected flock, the closest examination of 
the exposed birds should be made, so that those slightly infected may 
be isolated and treated. Otherwise they will perpetuate the infec- 
tion in the flock. Care should be exercised to prevent the introduc- 
tion of birds from flocks not positively known to be free from the 
disease. In an infected flock, thorough cleaning and disinfection 
of the quarters should be carried out. 



REFERENCES 

1. Balfour. Aspergillary pneumokoniosis in the lung of a turkey. 
Fourth Rep. Wellcovie Research Lab., 1911. 

2. Beach and Halnin. Observations on an outbreak of favus. J. Agric. 
Research, Vol 15, 1918, p. 415. 



ASPEEGILLOSIS 119 

3. Lignieres et Petit. Peritonite aspergillaire des dindon. Rec. de 
Med. Vet, T. 75, 1898, p. 145. 

4. Lucet De V Aspergillus fumigatus chez animaux domestiques et 
dans les oefs en incubation. Paris, 1897. 

5. Matruehot et Dassonville. Recherches experimentales sur une der- 
matomyeose des poules et sur son parasite. Rev. Gen. de Bot., T. XI, 
1899, p. 430. 

6. Mohler and Buckley. Pulmonary mycosis of birds. U. S. Dep. Agr. 
Bureau Animal Indust. Circ. 58, 1904. 

7. Neumann. Aspergillosis in domesticated birds. J. Comp. Path, and 
Therap., Vol. 21, 1908, p. 260. 

8. Sabouraud. Le trichophyton de la poule et la maladie humaine qu'il 
determine. Arch, de Med. Experim., Mai 1909. 

9. Sabouraud, Suis et Suffran. La " crete blanche " (favus) de la poule 
et son parasite. Rev. Vet., T. 34, 1909, p. 601. 



CHAPTER XI 

INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 

Si/)ionym. Blackhead. 

Characterization. Entero-hepatitis is an infectious disease of 
turkeys and fowls, characterized by distention of the ceca with ne- 
crotic material and the formation of yellowish or yellowish-green ne- 
crotic areas in the liver. 

Geographic distribution. It is widely distributed over the 
United States, and has also been reported from Canada, Europe, Aus- 
tralia and Africa. 

Etiology. The causative organism as described by Smith belongs 
to the genus ameba and has been designated by him Ameha mele- 
agridis. Through the researches of Hadley, the rule of an ameba in 
the causation is disputed. The latter investigator asserts that a fla- 
gellated protozoal organism, Tricliomonas, is the causative agent and 
that the organism described by Smith merely represents a transitory 
stage in the life cycle of the flagellate. The difticulties to be met 
with in establishing the etiologic factor of this disease are far greater 
than is the case in bacterial affections. In routine examination of 
entero-hepatitis cases by the present writers, it has been observed that 
flagellate forms are frequently present in the cecal exudate of tur- 
keys dead of entero-hepatitis while more often protozoal organisms 
of the ameba type are seen in comparatively large numbers. Fur- 
ther and more extensive investigation appears to be necessary in order 
to establish firmly the specific etiology of this disease. 

The organism described by Smith is round or oval in form with 
a single contoured outline. The structure appears homogeneous 
throughout with the exception of a small granular area eccentrically 
located and representing the nucleus. This encloses a smaller 
rounded body distinguished as the nucleolus. The protozoa in fixed 
or hardened tissue are from 6 to 10 microns in diameter, in fresh 
smears from 8 to 15 microns in diameter. 

The organism attributed by Hadley as the causative agent is a 
flagellate. This is most easily recognized in the motile stage. In 
this form it presents an irregular outline. It may be pear shaped, 
ovoid, triangi^ilar or elliptical in form. It has three anterior fla- 

120 



INFECTIOUS ENTERO-HEPATITIS OF TUKKEYS 121 

gella, a vibratory membrane and one posterior flagellnm. The nu- 
cleus is placed anteriorly. One or more food vacuoles may be ob- 
served. The average length of this form is about 10 microns. 

Pathogenicity. Young turkeys are especially susceptible, al- 
though there appears to be no period of immunity to primary in- 
fection during the life of the bird. The greatest losses occur during 
the first two or three months of life. Practically all of the exposed 
poults contract the disease at this time. Young chickens are only 
slightly susceptible but may serve as carriers of the organism. 

Source of infection. The disease is principally spread through 
exposure to infested ground. Once the causative agent has been 
brought on the premises, it is apt to continue its activity year 
after year. Whether this is wholly due to the resistance of the 
encysted stage of the parasite, to climatic or other external influ- 
ences or whether it is perpetuated in the intestinal tract of compara- 
tively resistant turkeys or chickens is open to speculation. From 
the fact that mature turkeys may show symptoms of entero-hepatitis 
during all seasons of the year, it is reasonable to assume that they 
constantly harbor the organism in a saprophytic form and only de- 
velop the disease as a result of adverse conditions or weakened con- 
stitution from other causes. Curtice states that chickens though 
rarely infected may serve as carriers. In any case, the disease is 
contracted by the poults ranging on ground infested by the droppings 
of carriers of the parasite. The parasite passes from the intestine in 
the encysted or resistant stage. In this form when not exposed to 
the direct rays of the sun or to considerable drying it may retain its 
vitality for a long period, possibly one to two years. Earth worms 
may play some part as mechanical carriers of cysts which have sur- 
vived in the soil under favorable conditions. When these encysted 
forms are taken into the alimentary tract by poults in feeding, they 
undergo changes which renew their activity. The tough resistant 
covering is discarded and forms developed from the central granular 
mass or nucleus penetrate the mucosa of the intestine, especially the 
ceca and may be carried by the blood stream to the liver. The para- 
sites multiply rapidly in the intestine and are passed out in enormous 
numbers in the droppings. By this means, other susceptible birds 
in the flock are directly infected through coming in contact with the 
contaminated material in feeding. 

Symptoms. The symptoms of entero-hepatitis become apparent 
within a period of four weeks after exposure. Young birds show 
less resistance and develop manifestations earlier than grown ones. 



122 DISEASES OF DOMESTICATED BIKDS 

The disease runs a rapid course in the former and deaths may 
follow in a few days. Older turkeys, fatally affected, usually suc- 
cumb within four weeks after the onset of symptoms. The mortality 
approaches 90 per cent in poults and 10 per cent or more in the 
gro^vn birds, according to the extent of exposure. Affected poults 
exhibit a drowsy attitude with constantly increasing lack of vigor. 
They are unable to keep up with the flock in its daily travel over 
large areas. The appetite is diminished, the feathers ruffled, wings 
are pendant, and a general air of debility is manifested. Diarrhea 
is nearly always present and quite characteristic. The droppings 
are soft and yellowish in color or may be mixed with brownish ex- 
crement. During the later stages the head may present a darkened 
or purple appearance due to impaired circulation of the blood. 
This symptom has led to the disease being termed " blackhead." 
However, this term is misleading since the darkened appearance 
of the head is not a constant svmptom and may also be observed in 
other diseases which lead to a weakened heart action. In older 
turkeys the symptoms are less pronounced and may be of much 
longer duration. They show loss of appetite, unthrifty appearance, 
lessened activity, progressive emaciation and diarrhea, with soft 
yellowish droppings. The disease may persist for a period of two 
weeks to two months and result fatally or the bird may regain its 
normal condition. Relapses frequently occur during the following 
year. The disease is more prevalent during the late summer or 
fall in young poults but may occur at any season and is frequently 
reported among grown turkeys during the winter and spring. 

Morbid anatomy. The lesions of entero-hepatitis are confined 
to the intestine and liver. In the intestinal tract the ceca are the 
principal seat of infection. In many cases only one cecum exhibits 
macroscopic alterations but quite frequently both ceca are equally 
involved. The walls become greatly thickened and covered by a 
necrotic exudate which completely fills the cavity or leaves but a 
small central space. The accumulation of exudate gives rise to a 
marked distention of these blind pouches plainly apparent when 
the intestine is exposed at autopsy. The exudate is dull gray in 
color and of a friable or cheesy consistency. The entire length of 
the cecum may be involved or only a limited area, depending on the 
severity or duration of the morbid process. In the majority of 
cases the liver is found infected to a greater or less degree. The 
lesions are characteristic. Areas of degeneration appear on the sur- 
face in circular form and of varying size. They are usually about 



INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 123 

Ys to % of an inch in diameter and may be isolated and few in num- 
ber or numerous and closely associated, even coalescent. Their color 
varies from a yellowish to a yellowish-green. These areas of ne- 
crosis extend more or less deeply into the structure of the liver and 
result from plugging of the smaller arterioles with the parasites and 
cellular debris. They are not always of a homogeneous color, but 
may appear mottled with small areas of approximately normal liver 
tissue. No elevation above the liver surface is in evidence as may 
be the case in tuberculosis or sarcomatosis of the liver and the tend- 
ency is rather to a slight depression beneath the capsule. The liver 
is often enlarged to a considerable degree and congested. 

In very acute cases the ceca show slight evidence of exudate but 
are more or less inflamed while the liver is free of lesions. Other 
areas of the intestine, especially the duodenum and rectum, harbor 
the causative parasite and may exhibit congestion of the mucous 
membrane, hemorrhagic points or even spots of necrosis. However, 
the ceca and liver are the main seats of disease and more to be 
relied upon for diagnostic evidence. Infrequently the morbid process 
within the lumen of the cecum extends through the mucosa, sub- 
mucosa, muscular layers and serous coat causing perforation and exu- 
dation into the peritoneal cavity leading to peritonitis or extensive 
adhesions of the cecum to the surrounding loops of intestine. This 
condition is apparently due to the action of invading bacteria since 
the protozoal organisms have not been demonstrated in these sec- 
ondary lesions. 

Microscopically the cecal exudate is found to be composed of 
protozoal bodies, exfoliated mucosa cells in various stages of degen- 
eration, connective tissue shreds, blood cells and an amorphous de- 
tritus. The cecal wall is greatly thickened due to infiltration and 
connective tissue hypertrophy. The mucosa shows extensive de- 
generative changes or is absent in areas. Depending on the depth 
of the ulceration, the circular or longitudinal muscular layers show 
more or less infiltration with small round cells and congestion, which 
may extend to the serosa. In the liver the necrotic foci show vary- 
ing stages of cell degeneration and are surrounded by a congested 
area. Walling off of the affected spots is not well marked or is 
totally absent. Small round cells, protozoal organisms and nuclear 
remnants are distingiiished in the amorphous necrotic material. In 
both the intestinal membrane and in the liver the protozoa occur 
either singly or in groups between the epithelial, or parenchymatous 
cells where they may be enclosed in a connective tissue network. 



124 DISEASES OF DOMESTICATED BIKDS 

Thej have also been observed in the interior of giant cells (Smith), 
and epithelial and endothelial cells (Hadlej). 

Diagnosis. Entero-hepatitis is readily differentiated from other 
diseases bv the definite character of its internal manifestations. 
The presence of yellowish or yellowish-green spots on the surface of 
the liver is specific. Turkeys are much less frequently alfected 
with tuberculosis, or malignant tumors than fowls and these dis- 
eases may be eliminated where several birds in a flock become in- 
fected at the same time, especially in the case of poults. The lesions 
of tuberculosis, on cut section, present a fleshy appearance whitish in 
color with yellowish points and usually extend to the spleen, intestine 
and mesentery where they appear as rounded nodules. Tumor 
formations vary greatly in size, are fleshy in character and are usu- 
ally found on the serous membrane. They are of a chronic cliar- 
acter and occur sporadically. In tuberculous infection, tubercle ba- 
cilli will be found in large numbers on microscopic examination of 
smears from the nodules. 

Treatment. Extensive experiments looking to the treatment of 
entero-hepatitis have so far failed to develop a satisfactory method. 
The insidious nature of the affection and the deep seated location 
of its parasite in the wall of the intestine and in the liver render 
it practically immune from interference by curative agents. . Eme- 
tin hydrochlorid, a derivative of ipecac, by repeated hypodermic 
injection has given more or less satisfactory results in the treat- 
ment of amebic dysentery in man, a disease somewhat analogous 
to entero-hepatitis of turkeys. However, the above disease of man 
is- of a chronic nature and lends itself to a more prolonged course 
of treatment than is permitted in the case of the comparatively acute 
disease under consideration. Also the value of young turkeys does 
not justify the time and expense which would be involved even were 
the treatment fairly successful. Giving ipecac in small doses might 
prove beneficial. The most promising and economical treatment is 
the administration of crude catechu by means of the drinking water. 
This has been recommended by Fantham for coccidiosis of fowls 
and has given good results in our experience. One-third teaspoon- 
ful of crushed crude catechu is added to each gallon of water. It is 
quite possible that the use of catechu in this manner during the first 
three months would bring the exposed poults safely through the most 
dangerous period. Should signs of constipation develop as a result 
of this treatment, the entire flock may be given Epsom salts in the 
proportion of one teaspoonful to every ten poults. The salts can 



INFECTIOUS ENTERO-HEPATITIS OF TURKEYS 125 

be dissolved in water and the solution mixed with a feed to be given 
early in the morning. Turkeys on range would require special at- 
tention for the successful operation of the above measures. Isola- 
tion or disposal of birds showing symptoms of disease is of the first 
importance in guarding against a further spread of the malady. 
Thorough cleaning and disinfection of quarters and yards will tend 
to keep the outbreaks in check. Carbolic acid in 5 per cent solution, 
or compound cresol in 3 per cent solution are efficient disinfectants. 

Prevention. Prevention of entero-hepatitis in infected com- 
munities is more difficult than the prevention of other diseases of 
domesticated birds, because of the fact that turkeys range over an 
area of several miles in diameter when allowed to rvm at large as is 
the usual custom in this country. The possibility of healthy flocks 
becoming infected by feeding on ground contaminated by diseased 
flocks is very apparent and renders preventive measures under such 
conditions rather difficult of execution. Where turkeys are con- 
fined to a limited area or do not come in contact with other flocks 
which harbor the parasite, simple precautionary measures may in- 
sure freedom from the disease. The main channel of entrance is 
through the introduction of birds which come from infected flocks. 
Particular care in selecting purchased birds should be exercised. 
The fact should be established beyond doubt that they are of a 
flock which has shown no symptoms of disease and have not been 
associated with neighboring diseased flocks. A period of quarantine 
extending over 30 days is also advisable before newly acquired tur- 
keys are placed with the home flock. 

Where the disease has been prevalent on premises to such an ex- 
tent as to make the raising of turkeys unprofitable, it is advisable 
to dispose of the entire lot and allow a period of approximately twn:) 
years to elapse before restocking. Local conditions may modify or 
suggest preventive measures. Limeing or plowing the runs or home 
feeding yards is indicated. The principal fact to be considered is 
that the disease must first be introduced, either by infected birds 
(almost invariably the turkey) or by mechanical carriers, such as 
persons coming from infected farms and carrying the causative par- 
asite on their shoes. Wild birds may possibly serve as carriers. 
Other agencies could be mentioned by means of which the organism 
of entero-hepatitis might be carried from infected farms ; however, 
these are of minor importance and cannot easily be guarded against. 
Eggs for hatching, from infected turkeys may be dipped in 95 per 
cent alcohol to destroy any parasites which may have become at- 



126 DISEASES OF DOMESTICATED BIEDS 

tached to the shell. Practically the only danger in using eggs from 
infected flocks is that the shells may have come in contact with drop- 
pings harboring the infectious parasite. 

On first indication of the presence of entero-hepatitis the affected 
birds should be destroyed and their carcasses burned or deeply 
buried. The quarters should be thoroughly cleaned and disinfected 
with 5 per cent carbolic acid or compound cresol in 3 per cent solu- 
tion. The runs or local feeding ground should be cleaned and 
limed or plowed under as the chance for infection is greatest at the 
points where the flock congregates most often. The confinement of 
turkeys to inclosed yards has been tried with apparently favorable 
results. By this method of rearing, entero-hepatitis could be more 
easily controlled. 

Hadley regards the prevention of Trichomonas infection in tur- 
keys as presenting a somewhat different problem from that involved 
in the prophylaxis of many diseases. The parasites are found nor- 
mally present in the intestines of all poultry. Their pathogenic 
activity in turkeys, in his opinion, depends upon factors present 
in the host which are probably quite unrelated to virulence on the 
part of the infecting organism. This view would suggest the exer- 
cise of great care in feeding in order to preserve health even though 
the flagellates are present in the intestine. 

REFERENCES 

1. Curtice. Notes on experiments with blackhead of turkeys. U. 8. 
Dep. Agr. Bureau Animal Indust. Circ. 119, 1907. 

2. Curtice. The rearing and management of turkeys with special refer- 
ence to the "blackhead" disease. Rhode Island Agr. Exp. Sta. Bull. 123. 

3. Curtice. Further experiments in connection with the blackhead dis- 
ease of turkeys. Rhode Island Agr. Exp. Sta. Bull. 12^. 

4. Cushman. Nature of blackhead in turkeys. Rep. Rhode Island Agr. 
Exp. Sta. 1894. 

5. Hadley. Blackhead in turkeys. A study in avian coccidiosis. 
Rhode Isla77d Agr. Exp. Sta. Bidl. Ul. 

6. Hadley. The role of the flagellated protozoa in infective processes 
of the intestines and liver. Rhode Island Agr. Exp. Sta. Bull. 166. 

7. Milks. A preliminary report on some diseases of chickens. Louisi- 
ana Agr. Exp. Sta. Bull. 108. 

8. Moore. The direct transmission of infectious entero-hepatitis in 
turkeys. TJ. S. Dep. Agr. Bureau Animal Indust. Circ. 5, 1896. 

9. Smith. Infectious entero-hepatitis in turkeys. U. 8. Dep. Agr. 
Bureau Animal Indust. Bull. 8, 1895. 

10. Smith. Further investigations into the etiology of the protozoan 
disease of turkeys known as blackhead, entero-hepatitis, typhlitis, etc. 
J. Med. Res., Vol. 33, 1915, p. 243. 



CHAPTEK XII 

COCCIDIOSIS 

Characterization. Coccidiosis is primarily a disease of the in- 
testinal tract. In young chicks it may also affect the liver and 
in geese, the causative organism may be localized in the kidneys. 
It is one of the greatest scourges of fowls, pigeons and turkeys. 

Etiology. The organism causing coccidiosis is designated Ei- 
meria (Coccidium) avium and belongs to a class of protozoan para- 
sites known as sporozoa. The organism is included in the animal 
kingdom and reproduces by both sexual and asexual processes. The 
parasite was long known as Coccidium a u mm but owing to the rules 
of priority in zoological nomenclature, the familiar name of the 
genus C occidium has been replaced by Eimeria. 

In the oocyst or resistant stage, the one most easily recognized on 
microscopic examination of the intestinal contents, the protozoan 
generally appears as an oval body containing a central granular 
mass surrounded by a highly refractile zone with a double con- 
toured border. The size varies from 25 microns to 35 microns in 
length and from 15 microns to 20 microns in breadth. 

Life history of Eimeria avium. The life history has been ad- 
mirably worked out by Fantham. There are two principal stages in 
the life cycle, a stage of asexual multiplication, termed schizogony, 
and a stage of sexual reproduction in which male and female elements 
unite to form resistant bodies for life outside the animal cells. In 
the asexual stage the newly formed parasites pass from one cell to 
another, and it is during this cycle that the great destruction of in- 
testinal mucosa occurs. 

(a) The young, growing parasite. The oocyst reaches the duo- 
denum of the bird through the medium of the food or water. Here 
the tough cyst wall is softened and four small oval bodies or spores 
are released. From each of these are given off two actively motile 
vermiform bodies with one end more pointed than the other, which 
vary from 7 to 10 microns in length. These are the primary infect- 
ing germs or sporozoites (fig. 13 A). The sporozoite passes into an 
epithelial cell lining the first portion of the intestine where it curls 
on itself (fig. 13 B), takes on a spherical outline (fig. 13 C) and be- 

127 



Fig. 13. Diagram of life 
cycle of Eimeria (cocci- 
dium) avium. (Fantham) 

B-H. Illustrate the asex- 
ual reproduction (scliizog- 
ony) of E. avium. Epithe- 
lial host cells diagrammat- 
ically outlined. 

I-L. Illustrate the pro- 
duction of sexual forms 
( gametogony ) . 

N-T. Illustrate spore 
formation ( sporogony ) . 

A. Sporozoite or primary 
infecting germ wliicli pene- 
trates the epithelial cell of 
the duodenum of the host. 

B. Sporozoite curving on 
itself before becoming 
rounded within the host 
cell. 

C. Young, growing para- 
site. 

D. Fully grown parasite 
(Trophozoite) . 

E. Schizont, with numer- 
ous daughter nuclei peri- 
pherally arranged. ( Seen 
in transverse section.) 

F. Schizont, showing far- 
ther differentiation of mero- 
zoites. 

G. Merozoites arranged 
" en barillet," about to issue 
from the host cell. 

H. Free merozoites. 
I ? . Young macrogame- 
tocyte with coarse granules. 

Id. Young microgametocyte with fine granules. 

J9. Growing female mother cell, showing chromatoid and plastinoid granules. 
^ JcT. Microgrametocyte with nucleus divided to form a number of bent, rod- 
like portions, the future microgametes. 

K?. Macrogamete which has formed a cyst wall for itself but left a thin 
spot for the entry of the microgamete. 

Kef. Microgametocyte with many biflagellate microgametes about to separate 
from it. 

L. Fertilization. One microgamete is shown penetrating the macrogamete, 
while other male cells are near the micropyle but will be excluded. 

M. Fertilization. The male pronucleus is lying above the female chromatin. 
Degenerating microgametes are shown outside the oocyst. 

N. Oocyst (encysted zygote) with contents filling it completely. 

0. Oocyst with contents concentrated, forming a central, spherical mass. 
Many such cysts seen in infected cecal droppings. 

P. Oocyst with four nuclei. 

Q. Oocyst with contents segmented to form four rounded sporoblasts. (As 
seen in fresh preparations.) 

R. Oocyst with four sporoblasts which have grown oval and are becoming 
sporocysts. 

S. Oocyst with four sporocysts, in each of which two sporozoites have dif- 
ferentiated. 

T. Free sporocyst in which the sporozoites have assumed the most suitable 
position for emergence. 

128 




COCCIDIOSIS 129 

gins to grow in size at tlie expense of the host celh This is known as 
the trophozoite stage (fig. 13 D). 

(b) Asexnal multiplication or schizogony. When fully developed 
the trophozoite has a diameter of 10 to 12 microns. In preparation 
for propagation the nucleus divides into a number of daughter nuclei 
which arrange themselves in a zone at the periphery. This consti- 
tutes the schizont stage and represents the beginning of asexual mul- 
tiplication or schizogony (fig. 13 E). Each nucleus becomes sur- 
rounded with protoplasm and assumes a long narrow form with 
pointed ends. The length ranges from 6 to 10 microns (fig. 13 F G). 
These bodies, known as merozoites, differ from sporozoites in that 
their nuclei contain a small particle of chromatin, the karyosome. 
From 8 to 20 merozoites are formed from 1 schizont. On separation 
from one another (fig. 13 H), the merozoites work their way into 
other cells, lining the intestinal tract and may repeat the process 
of development just outlined, or differentiation into sexual forms 
may take place within the newly invaded cells. This process is 
termed gametogony. 

(c) Sexual reproduction or gametogony. Two forms of the or- 
ganism are now produced, the macrogametocyte or female mother 
cell (fig. 13 I J) and the microgametocyte or male mother cell (fig. 
13 I J). Both forms are oval in shape, the former being somewhat 
larger and more granular than the latter. Also the former gives 
rise to only one daughter cell or macrogamete (fig. 13 K) while 
the latter produces a large number of minute, biflagellate, actively 
motile male cells or microgametes (fig. 13 K). The macrogametes 
are from 11.8 to 17.5 microns in length and 6 to 11 microns in 
breadth, in sections. The microgametes are 3 to 4 microns in length, 
in sections. 

(d) Fertilization. Fertilization takes place through the entrance 
of the microgamete or male cell into the structure of the female 
cell or macrogamete at the thin spot at one end known as the mi- 
cropyle (fig. 13 L). After the entrance of the male cell the macro- 
gamete secretes protoplasm which plugs the opening and prevents 
the entrance of other microgametes. On union of the nuclei of the 
two gametes, a zygote is formed which proceeds to spore formation or 
sporogony (fig. 13 M IST). 

(e) Sporogcmy. The zygote is surrounded by a tough double con- 
toured membrane which is extremely resistant. This stage is kntiwn 
as the escii; stage, or oocyst. The contents arc at first granular and 
grayish in appearance (fig. 13 'N). Later the granular material is 



130 DISEASES OF DOMESTICATED BIRDS 

gathered into a compact circular mass approximately in the center 
of the oocyst (fig, 13 0). The nucleus imbedded in the central mat- 
ter now undergoes division into two and these in turn divide, form- 
ing four daughter nuclei (fig. 13 P). These are surrounded by cyto- 
plasm and separated from each other. As a result four rounded 
bodies are formed within the cyst. These are sporoblasts (fig, 13 Q). 
Later the sporoblast loses its rounded form, becomes oval and is 
inclosed in a cell wall (fig. 13 R). In this form it is termed a 
sporocyst and from it develops a spore which contains two young 
infective parasites or sporozoites. The life cycle is completed by 
the rupture of the oocyst wall in the intestinal tract of the host, 
which releases the spores and the primary infecting sporozoites. 

From experiments made by feeding fowl chicks with coccidian 
oocysts, Fantham concUides that the period for the total life cycle 
of the parasite is from eight to ten days. 

Pathogenicity. Apparently coccidiosis is infectious to all do- 
mesticated and wild birds which are exposed to its causative organ- 
ism. It has been observed in a wide variety of these birds and its 
incidence has been marked by high mortality, especially in those con- 
fined to limited areas. It is highly destructive to young chickens 
and frequently affects baby chicks. Its gTeatest ravages are seen 
in chickens which have passed the brooder stage and are exposed 
to the infective agent in infected houses or grounds. Limited range, 
as is customary in the rearing of domesticated birds, and especially 
in the case of chickens closely confined in large fiocks, is conducive 
to heavy infection and high mortality in the event that coccidia are 
present. Next to chickens, pigeons are no doubt most severely af- 
fected. Outbreaks among ducks and geese occur less often as an 
epizootic unless the birds are closely confined, but individual infec- 
tion commonly occurs. 

Birds of all ages are susceptible. Mature birds exhibit a fair de- 
gree of resistance. They may harbor the coccidia and appear nor- 
mal until they become grossly infected, or become weakened through 
other causes to such an extent that their power of resistance is lost. 

Mortality. In chicks affected at the age of two to ten weeks, 
the disease runs a rapid course and the mortality may reach 100 per 
cent in closely confined flocks. In older fowls, the fatalities, while 
not so great, are usually very heavy in those surrounded by unsan- 
itary conditions. Mature hens have a greater power of resistance 
but even among these, severe losses may be observed. The mortality 
is governed by the degree of exposure. 



COCCIDIOSIS 131 

Course of the disease. The coccidium when once introduced into 
a flock develops rapidly in the cells of the intestinal mucosa^ giving 
rise to a great number of sexual and asexual forms which are passed 
out in the droppings and are ingested by healthy birds. Accumu- 
lation of infected droppings naturally tends to increase the number 
of these organisms ingested and results in gross infection. Where 
fairly good sanitary conditions are maintained, the spread of the 
disease is less general and the amount of infectious material con- 
sumed is proportionally lessened. As a result, birds which have a 
degree of normal resistance are protected against heavy infection. 

Symptoms. The outward manifestations of coccidiosis depend 
to a considerable degree upon the age of the birds attacked. In 
young chicks, the disease develops rapidly and the mortality is high. 
The affected ones display the usual appearance associated with de- 
bilitating internal disorders, such as weakness, disordered feathers, 
droopy wings, bunched appearance, loss of appetite, and somnolence. 
The droppings are semi-fluid and usually whitish in color, but may 
be of a fluid nature with brownish tinge. In very acute cases in 
young chicks the droppings are deeply stained with blood. Affected 
chicks of an age of three weeks or less to two months seldom survive 
in a severe outbreak and those that recover are stunted and worthless. 
Chicks affected fatally succumb in from one to several days after out- 
ward symptoms are apparent, depending upon their age. The older 
ones show a stronger resistance, but in these too, the fatalities are 
extremely heavy. 

In grown fowls, the disease usually assumes a more chronic type, 
although acute outbreaks are not infrequent. In these acute out- 
breaks, the affected birds show the droopy appearance which is more 
or less characteristic of all infectious diseases of fowls, and which, 
in itself, has comparatively little value as a diagnostic feature. In 
semi-acute cases, the fowl develops a progressively increasing list- 
lessness and loss of activity. The comb becomes pale and periods of 
dejection, during which the bird stands in an isolated position, in- 
crease as the disease progresses. The appetite may remain normal 
and is frequently ravenous when the fowl is aroused at feeding time. 
During intervals between regailar feeding, there is little effort to 
scratch for food with the others of the flock. The symptoms may be 
apparent for from one to three weeks, death occurring quite sud- 
denly or after a short period of coma. In the more chronic form, 
the fowl retains a pale appearance of the comb and wattles for 
several weeks, the appetite appears nonnal while the bird is eating, 



132 DISEASES OF DOMESTICATED BIRDS 

but the amount of food consumed is less than usual, owing to the 
general indifference to food during prolonged intervals. Emacia- 
tion is marked both in semi-acute and chronic cases, principally due 
to the fact that the destruction of the lining membrane of portions 
cf the intestine prevents normal assimilation of the food. Leg 
weakness and paralysis are frequently observed. 

Affected geese become gi-eatly weakened and emaciated. After 
walking a few steps they will fall and after a struggle roll on their 
backs, a position which is frequently assumed. 

Morbid anatomy. The lesions are principally confined to the 
intestinal tract and are most noticeable in the ceca, in chickens and 
turkeys. In young chicks in which the disease assumes an acute 
course, the ceca are filled with a bloody semi-solid mass which shows 
through the intact tubes and gives them a distended contour. This 
mass consists of blood cells, exfoliated mucosa, fecal matter, and ex- 
tremely numerous coccidial forms of which the oocysts or egg forms 
are especially apparent on microscopic examination. In older fowls, 
the ceca may be distended to a greater or less degree. In the ma- 
jority of eases, the distention is marked and the tubes are firm to the 
touch over a considerable extent of their length. Hemorrhagic areas 
may show through the serous membrane, or the affected parts may ap- 
pear pale and deadened. One cecum only may give evidence of mor- 
bid changes, but as a rule both are equally affected. On incision, 
the lumina are found packed with a solid necrotic mass of a grayish 
color and cheesy consistency. The mucous membrane is completely 
degenerated and forms a part of the caseatcd mass. On microscopic 
examination, the necrotic material appears as an amorphous mass 
in wdiich mucus, cells in various stages of degeneration, food material 
and numerous coccidial cysts are incorporated. The mucous lining 
of the duodenum is invariably the seat of pathologic changes and is 
the portion of the intestine first affected. In many instances, this 
is the only part which shows lesions on post-mortem examination. 
The lining membrane is deeply congested, or hemorrhagic. 

Diagnosis. Coccidiosis is readily diagnosed by a microscopic 
examination of the droppings of infected birds, or of the intestinal 
contents at autopsy. A small amount of the material is broken up in 
several drops of a 1 per cent potassium hydrate solution, normal 
salt solution, or water and about two drops of the mixture are placed 
on a glass slide and a cover glass applied. The coccidia usually 
are very numerous in advanced cases and are easily recognized in 
the oocyst or resistant stage. They have an oval appearance with 



COCCIDIOSIS 133 

a central, rounded, darkened area surrounded by a wide, clear', 
transparent zone with double contoured border. Other stages of de- 
velopment may be observed, however, the oocyst form is most easily 
recognized. Symptomatically the disease may be confused with ba- 
cillary white diarrhea and aspergillosis in young chicks, and with 
tuberculosis, aspergillosis, and infectious leukemia in older fowls. 
It is differentiated from bacillary white diarrhea by the fact that 
deaths from the latter occur principally within the first three weeks 
of life, while coccidiosis usually appears at a later period. As- 
pergillosis occurs more rarely and is generally restricted to a rela- 
tively small number of the flock. It is easily differentiated from 
coccidiosis on post-mortem examination by the localization of its 
lesions in the air passages, especially in the air sacs of the abdomen. 
Tuberculosis is readily distinguished by its characteristic nodular 
formations in the liver and intestines, or by microscopic examina- 
tion. In infectious leukemia, the liver is enlarged and usually 
studded with small necrotic spots while the ceca are free of masses 
of caseated material. 

Treatment. Attempts at treatment have not given very satis- 
factory results owing to the highly resistant powers of the organism 
during certain stages of its life cycle and to the position which it 
occupies in the intestinal membranes. Crude catechu, recommended 
by Fantham, has, in our experience, proved more effective than other 
preparations which have been recommended. The most convenient 
method of administration is by means of the drinking water. The 
lumps should be broken up by grinding or pounding into a coarse 
powder and added to the water in the proportion of Vs teaspoonful 
to each gallon of water. This solution is to be kept constantly avail- 
able to the flock while the disease is prevalent. Should signs of 
constipation develop, the entire flock may be given a dose of Epsom 
salts in the proportion of Vs teaspoonful to each adult fowl. The 
salts can be dissolved in water and mixed in a mash. The purgative 
effect is greatest if the mash is fed in the morning when the crop 
contains a minimum amount of food. It is advisable when s\anp- 
toms of coccidiosis are first noticed to give the flock a dose of Epsom 
salts before the crude catechu treatment is started. Where catechu 
is not available, bichloride of mercury may be substituted. It is 
given in the drinking water in the strength of 1 to 6000. Perman- 
ganate of potash 1 part in 500 parts of drinking water has also 
proved effective. 

Prevention. Once this disease has been introduced, the most sat- 



134 DISEASES OF DOMESTICATED BIRDS 

isfactorj method of combating it is through preventive measures 
against its spread. Birds showing symptoms should be isolated im- 
mediately, the houses thoroughly cleaned, and the floors, dropping 
boards and roosts soaked with carbolic acid in 5 per cent solution, 
or crude carbolic acid, or compound cresol, in 2 per cent solution. 
Other disinfectants, especially the coal tar prodvicts, may be substi- 
tuted, provided sufficiently strong solutions are applied. The dis- 
infectant may be spread by means of a spray pump or brush, but it 
is important that the places exposed to droppings should be covered 
by the fluid. During the course of an outbreak the droppings are 
to be removed frequently as it is through these that the infection 
is passed to healthy birds while feeding in contaminated pens. Runs 
to which diseased fowls have had access are highly dangerous to the 
non-infected and should be abandoned for a year at least if possible. 
These may be plowed and seeded, or if their use as runs is impera- 
tive the soil may be limed and plowed under. Since earth worms are 
credited with serving as hosts of the coccidium, stringent measures are 
necessary on badly infected premises, to accomplish complete eradi- 
cation of the disease. Covering the ground with chloride of lime or 
unslacked lime at intervals may prove sufficient, especially where 
preventive measures have been adopted early and a minimum ex- 
posure to infested droppings is indicated. Fowls received from out- 
side sources, unless known to be unexposed, should be quarantined 
for a period of three to four weeks before being placed in the flock. 

REFERENCES 

1. Fantham. Experimental studies in avian coccidiosis. Proc. Zool. 
Soc. London, Vol. 3, 1910, p. 708. 

2. Fantham. Coccidiosis in British game birds and poultry. /. Econ. 
Biol, Vol. 6, 1911, p. 75. 

3. Jowett. Coccidiosis of the fowl and calf. J. Comp. Path, and 
Therap., Vol. 24, 1911, p. 207. 

4. Meyer and Crocker. Some experiments on medical treatment of 
coccidiosis in chickens. Am. Vet. Rev., Vol. 43, 1913, p. 497. 



CHAPTEE XIII 

SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 
SPIROCHETOSIS 

Synonyms. Fowl fever, spirillosis of fowls, spirillose des poules, 
Hiihnerspirillose. 

Characterization. Spirochetosis is an acute, highly fatal, fe- 
brile, septicemic disease of birds caused by spirochetes and trans- 
mitted by fowl ticks. 

Geographical distribution. The disease has been reported in 
ISTorth and South Africa, India, Australia, Russia, Hungary, Rou- 
mania, Bulgaria, Cyprus, South America and the West Indies. 

The existence of the disease in the United States within the area 
of distribution of the fowl tick (See Fig. 53, p. 221) has been 
suspected by various writers, but so far as known its presence has not 
been definitely proven. Symptoms ascribed to excessive tick infesta- 
tion, such as paralysis, drooping of wings, ruffled feathers, loss of ap- 
petite and even death have suggested the idea that spirochetosis may 
be present. 

Etiology. 8 pirochceta (Treponema) gallinarum (S. march- 
ouxi) causes the disease in fowls, while 8pirochceta anserina has 
been identified as the cause of a similar infection in geese. Some 
consider 8. anserina as identical with 8. gallinarum. 

The general shape of a fully developed spirochete is that of a nar- 
row sinuous thread, in some cases reaching nearly 20 microns in 
length. The cells possess active motility. Spirochetes are generally 
regarded as protozoan organisms, although the belief that they are 
bacteria has many adherents. The organisms may be stained in 
blood films by fixing with osraic acid vapor, after which the films are 
hardened in absolute alcohol and stained with Giemsa or one of the 
modifications of that stain. Carbol fuchsin may be employed as a 
stain. 

ISToguchi has cultivated 8. gallinarum in a special medium de- 
vised to provide suitable conditions. An infected bird is placed 
under ether anesthesia and blood is drawn aseptically from the heart. 
To prevent coagulation the blood is mixed with an equal amount of 

135 



136 DISEASES OF DOMESTICATED BIRDS 

1.5 per cent solution of sodium citrate in a .9 per cent solution of 
sodium chlorid. A piece of kidney of a normal rabbit or a piece of 
pectoral muscle of a fowl is placed in a test tube. Ascitic fluid is 
added to make the column of fluid 10 cm. high or about 10 to 15 c.c. 
To this is added a few drops of the infected blood. The fluid is 
covered with a layer of paraffin oil that has been autoclaved twice. 
Ascitic fluid is not always suitable and it may be necessary to try 
many lots. 

The maximum growth is reached at about the fifth day, the cells 
being fully developed typical spirochetes. After the fifth day de- 
generation of the cells begins and proceeds slowly. The organism has 
been demonstrated to remain virulent for chickens through 13 gen- 
erations of culture. However, under certain cultural conditions it 
may lose its virulence. The inoculation of birds with such aviru- 
lent strains induces a resistance to subsequent infection with a viru- 
lent strain. 

Pathogenicity. Fowls, geese, ducks, guinea-fowls, turtle doves 
and sparrows have been reported as susceptible. Animals com- 
monly employed in laboratory work are immune, but Levaditi re- 
ports that he produced a transitory spirochetosis in a rabbit lasting 
three or four days. 

Poultrymen, when spirochetosis occurs, are apt to attribute losses 
to excessive tick infestation and to the resulting loss of blood with- 
out recognizing that an infectious disease is the cause of the losses. 

The prevalence of the disease will coincide with the season that 
is most favorable to the multiplication of ticks, but deaths will oc- 
cur at any time when susceptible stock is introduced, providing ticks 
are at all active. 

Bevan notes that birds in infected flocks become immune. How- 
ever, the birds previously immune will succumb after the introduc- 
tion of newly arrived susceptible birds starts the infection anew. It 
is possible that the passage through susceptible birds increases the 
virulence of the virus. 

Upon introduction of infection into a flock hitherto uninfected, 
spirochetosis may be exceedingly fatal and exterminate a flock in a 
few days. Young birds are particularly susceptible. 

The course of the experimentally produced disease varies accord- 
ing to the method of the introduction of the virus, the activity of 
the spirochetes and the receptivity of the bird. When the inocu- 
lation is made by means of the tick, after 6 to 8 days and sometimes 
more, the spirochetes are encountered in the circulation. If inocu- 



SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 137 

lation is made with virulent blood through the skin, the period of 
incubation is reduced to a period varying from 48 to 72 hours. The 
period of incubation is longer when the virus is placed on the skin 
superficially. 

The disease is acquired easily through the mouth, especially if the 
virulence of the parasite has been raised by a number of passages. 

Symptoms. Very commonly the disease occurs in such an acute 
form that birds apparently healthy at night are found dead under 
the roost in the morning. In the less rapidly fatal form there is 
dullness, ruffling of the feathers, somnolence and diarrhea. The 
comb becomes pale as a result of anemia. The temperature reaches 
110° or 112° F. but drops abruptly at the crisis, which coincides 
with the disappearance of the spirochetes from the circulating blood. 
During the course of the disease^ there is a marked decrease in the 
number of red corpuscles and a leucocytosis characterized by increase 
in the number of polynuclear leucocytes. After the crisis, the poly- 
nuclear cells diminish and the mononuclear cells increase in num- 
ber. The acute type of disease may be terminated by death in from 
four to five days- after the onset of symptoms. Death often occurs 
during convulsions. 

The chronic type may follow the acute phase or appear inde- 
pendently. Death may not occur for fifteen days. Paralytic symp- 
toms are noted. The wings may droop^ or the head be twisted back, 
or the legs may be involved. Inability to use the claws is an early 
sjTiiptom of leg paralysis. There may be disturbances of gait, and 
the bird may appear knock kneed or bowlegged. Emaciation and 
anemia are also particularly characteristic of the chronic type. 

Morbid anatomy. In birds dead of an acute attack, the spleen 
is found to be enlarged to several times normal. The liver also is 
greatly enlarged, shows fatty degeneration and sometimes focal ne- 
crosis. The other organs do not usually show marked lesions beyond 
the paleness of muscles, lungs and kidneys resulting from the ane- 
mia. The intestines sometimes are congested, and show punctiform 
hemorrhages. In chronic cases on the other hand, the liver and 
spleen are smaller than normal. 

The skin shows evidence of tick bites in the form of subcutaneous 
hemorrhagic areas. 

Microscopic examination of the blood of a bird dead of the disease, 
or during life after the crisis, will not reveal spirochetes. 

Life cycle of spirochetes. After the spirochete in the blood 
reaches a length of 16 to 19 microns it divides by a transverse divi- 



138 



DISEASES OF DOMESTICATED BIKDS 




Fig. 14. Various stages in the flexions and transverse divisions of Treponema 
( Spirochoeta gallinarum ) . ( Hindle ) 

sion. This is accomplished only after a series of movements con- 
sisting of doubling back on itself, coiling of the two portions, un- 
coiling and eventual separation. The process is illustrated in Fig. 
14, the successive stages of the process being indicated by the let- 
ters a to h. Sometimes the separation occurs as illustrated in e, 
but usually takes place after the position h is reached. Whether or 
not transverse division takes place directly without previous flexion 
has not been definitely determined. The act of uncoiling and sep- 
aration as illustrated in d, f, and g of Fig. 14 very closely sim- 
ulates a process of longitudinal division and has been erroneously so 
interpreted by some observers. The process of transverse division 
doubtless occurs repeatedly in the blood. 

Penetration of red blood cells and invasion by spirochetes has 
been observed but seems to be uncommon. 

At the time of the crisis of the disease, which is synchronous with 
the disappearance of spirochetes from the circulating blood, some 
spirochetes break up into a number of coccoid bodies in a manner 
analogous to the formation of spores within a bacterial cell. It is 
not certain that these coccoid bodies formed under the conditions in 
question redevelop into spirochetes within the blood of the fowl. 

Some of the spirochetes taken into the tick with a feeding of fowl 
blood, penetrate the wall of the gut and gain access to the coelomie 
fluid which occupies the body cavity of ticks. After a short time 



SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 



139 




MULTIPLICATION OF 
— COOCOIO BODIES 
IN CELLS OF ARQAS 




FORMATION OF 

COCCOID BODIES 

IN CELLS OF ARQAS 




Fig. 15. 



The life-cycle of Treponema {SpirocJueta) galUnaruni illustrated dia- 
grammatically. (Hindle) 



the spirochetes further penetrate into various organs of the tick, 
including the ovary and Malpighian tubules where they multiply 
by ordinary fission. In the cells of these organs the spirochetes 
break up into coccoid bodies. Other spirochetes remaining in the 



lumen of the- gut also form coccoid bodies. These circumstances 



re- 



140 DISEASES OF DOMESTICATED BIRDS 

suit in the infection of the Malpighian secretion and excrement with 
coccoid bodies. 

While the salivary gland has been considered with reference to the 
part played by saliva in introducing infection into fowls, the obser- 
vations tend to show that contamination of the tick-bite wound by 
coccoid bodies in excrement and coxal fluid, is responsible. 

Coccoid bodies are capable of development into the typical spiro- 
chete by a process of gi-adual lengthening. This has been observed 
in the ticks but not in the blood of a fowl. 

The eggs of an infected tick contain coccoid bodies and the progeny 
of such a tick is infective either by feeding on a fowl or when in- 
gested by a fowl. 

Ticks after feeding on infected blood are most liable to be in- 
fective when kept at a temperature of 30-35° C. When ticks are 
kept at 15-18° C, the spirochetes disappear from the alimentary 
tract, and such ticks do not transmit the infection. 

Differential diagnosis. The various septicemias of fowls, more 
particularly fowl cholera, might readily cause symptoms and lesions 
simulating spirochetosis. Microscopic examination of stained blood 
smears should furnish conclusive evidence by showing whether the 
septicemia is caused by spirochetes or by bacteria. The limited 
area of the United States in which ticks occur, see p. 221, should be 
borne in mind. 

Treatment. Dodd reports that /'s grain of soamin dissolved in 
one c.c. of sterile water and injected intramuscularly, modified and 
shortened the attacks with rapid and complete recovery, lllilen- 
huth gave atoxyl in an average dose of 5 centigrams at the time of 
infection or two days later. It prevented infection or cured but 
the blood remained infective. 

Hauer concludes that salvarsan is capable of destroying spirochetes 
in the body. The curative action of this substance is established 
in all cases on the day of treatment and acts in a remarkable manner 
even after the use of a limited amount of salvarsan. Even in cases 
where the treatment was first given on the fourth day after infection, 
when the bird was somnolent and when the blood was swarming with 
spirochetes, one injection of the agent in not too small a dose led to 
striking improvement and recovery. The immunity which salvarsan 
confers upon birds protected with it, is of high degree and of long 
duration. 

Hauer experimented on fowls with a wide variety of doses of 
the drug. The lowest lethal dose was found to be .3 gram and .15 



SPIROCHETOSIS AND RAEE INFECTIOUS DISEASES 141 

gram was the maximum dose tolerated. The curative dose on the 
second day of infection when spirochetes were observed in the blood, 
varied from .02 to .003 gram per kilo of body weight. Even the 
lowest dose caused the disappearance of spirochetes from the circu- 
lation and the birds recovered. Birds treated on the third day of 
infection received doses varying from .03 gram to .0025 gram per 
kilo of body weight. The lowest dose that uniformly caused the dis- 
appearance of the spirochetes was .005 gram per kilo. A dose of 
.05 gram per kilo was effective when administered to birds on the 
fifth day of infection. Aragao recommends atoxyl in a dose of .03 
gram, salvarsan .0035 gram and neosalvarsan in .0015 gram per 
kilo of body weight. 

Immunization. An attack of spirochetosis confers a certain 
amount of immunity. The blood serum of such a bird possesses 
strong immunizing properties and shows marked agglutinative action 
in vitro. 

Aragao induces immunity by injecting a vaccine prepared from 
the blood of infected fowls. On the fifth day of the infection the 
blood is drawn aseptically into flasks holding 300 c.c. each and de- 
fibrinated by shaking with shot. Blood drawings from the various 
fowls are mixed to secure a uniform distribution. The defibrinated 
blood is distributed in quantities of 50 c.c. each in flasks of a ca- 
pacity of 125 c.c. The flasks are plugged with cotton which has 
been dipped in formalin. The fluid is left thus exposed to the 
vapor of formalin for eight days and is shaken occasionally during 
that period. After carrying out suitable tests for sterility, it is in- 
jected subcutaneously in one c.c. doses for immunizing birds be- 
fore introduction into infected flocks. A similar product is pre- 
pared by Aragao by mixing defibrinated blood and glycerine in equal 
parts, omitting the formalin vapor treatment. It is used in two c.c. 
doses and is preferred to the one prepared by using formalin. A 
single injection is employed, for subsequent attacks by ticks in an 
infected flock are relied upon to strengthen the immunity. In unin- 
fected flocks where the vaccination is employed as a protection 
against imported infection only, revaccination is recommended once 
a year. 

Marchoux and Salimbini have observed that the virulence of the 
spirillum in blood is greatly diminished or lost after a period of about 
48 hours. They produce successful vaccination by using virulent 
blood held for two to four days, or after heating at 55° C. for five 
to ten minutes. 



142 DISEASES OF DOMESTICATED BIEDS 

Control of spirochetosis. The relation of fowl ticks to the 
spread of the disease is so direct, that the destruction of ticks is of 
necessity the first measure to be employed in combating the disease. 
See p. 223. Fowls not infested with ticks, but liable to become 
so, might be immunized with Aragao's vaccine. Susceptible birds 
before introduction into tick infected localities might be so im- 
munized. 

EARE INFECTIOUS DISEASES 
KABIES 

Several writers report the occurrence of rabies among fowls. Af- 
fected birds show restlessness and great fright. The feathers are 
ruffled and the bird attacks its fellows, other domestic animals and 
even man. 

Autopsy findings reveal no marked lesions. Injuries of the skin, 
foreign bodies in the gizzard together with congestion of the kidneys 
and intestines are conditions most frequently found. 

The prophylactic measures indicated are isolation of birds during 
outbreaks of rabies with slaughter of infected birds. 

Intracranial inoculation of fowls with rabies virus causes paraly- 
sis of the feet and neck, associated with uncertain gait. 

FOOT AND MOUTH DISEASE 

The occurrence of foot and mouth disease has been observed in 
fowls, waterfowl and pigeons but a few times. The lesions have 
been reported as occurring on the skin of the head, on the buccal 
mucous membrane and about the feet. 

Ehrhardt states that this disease is very rarely transmitted to 
fowls from cloven hoofed animals, for birds show a very high re- 
sistance to both natural and artificial infection. The disease is man- 
ifested by the occurrence of vesicles on the appendages of the head, 
on the mucous membrane of the mouth and throat as well as on the 
feet. In waterfowl the lesions appear mostly on the webs of the 
toes, and on the mucosa of the mouth and throat. In most cases the 
course of the disease is favorable and the lesions heal spontaneously 
in from eight to fourteen days without treatment. As a result of 
the cessation of eating, the affected birds appear weak and cease 
laying. In severe cases lameness and fever are observed followed 
by decline and death. 



SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 143 



MALTA FEVER IN FOWLS 

Dubois reports the occurrence of this disease in fowls. The out- 
break histed three months, with a mortality of 70 per cent. 

Symptoms. Birds of all ages are affected. The disease pre- 
sents two clinical forms: an acute or subacute form in which the 
duration is 8 to 10 days at the most, and a fulminating form lasting 
only a few hours. 

In the acute form the affected birds appear feeble, walk with dif- 
ficulty and display inappetence. After three or four hours the birds 
stop moving and appear depressed. The wings drop, the birds 
allow themselves to be caught easily, and sometimes show diarrhea 
with gi-een discharges. There is extreme emaciation at the last. 

In the fvilminating type few characteristic signs are observed. 
There is only weakness and depression. Some birds die suddenly 
without having shown symptoms. 

Morbid anatomy. In the fulminating type the lesions consist 
of ecchymoses on the lungs, a marked hypertrophy of the spleen and 
a certain degree of congestion of the liver. 

Inoculations made with the liver, the spleen, and heart blood of 
sick birds have given negative results. Likewise, inoculation of 
rabbit, guinea pig and pigeon with the pulp of the spleen and heart 
blood of sick birds has always failed to affect these animals. 

The writer determined the agglutinative properties against M. 
melitensis possessed by the blood of the affected birds. Of 8 fowls 
2-5 years old, 3 presented a positive reaction; of 9 birds 2-4 months 
old, 5 gave positive reaction. 

ANTHRAX 

Dawson points out that chickens may contract anthrax by eating 
the carcass of an animal dead of that disease. The disease runs a 
rapid and fatal course within 24 hours. The affected bird shows 
fever, high temperature, weakness, tremors and convulsions, together 
with bloody fecal discharges. Swellings may occur on the comb, wat- 
tles, sides of the head, in the mouth or on the feet. 

Mollhoff concludes that birds are more or less susceptible to in- 
oculation with anthrax. Exception is made in the case of hens, 
which in his experiments showed high resistance. Out of sixteen 
hens exposed by subcutaneous, intramuscular and intraocular in- 
jection, with doses as high as 2 c.c. or by feeding, only one sue- 



144 DISEASES OF DOMESTICATED BIRDS 

cumbed. This bird before inoculation was observed to be highly 
emaciated and anemic. Two geese receiving subcutaneous injections 
of 4 c.c. resisted infection. Of 16 pigeons inoculated, 7 contracted 
anthrax. Other birds such as ducks, sparrows, canaries, jays, hawks 
and crows, were very susceptible to inoculation. That writer makes 
a distinction between susceptibility to anthrax by inoculation, and 
susceptibility to the natural spontaneous infection. He knows of no 
instance of the latter. 

Mollhoff concludes that the resistance of the hen to anthrax con- 
sists of action of the body fluids or Ijanph by virtue of strongly 
bactericidal materials contained in them. The anthrax bacilli in 
the subcutaneous tissues are killed in a short time by the bacteri- 
cidal action of the lymph, so that no local development nor general 
infection can occur. 

The origin of this bactericidal material of the lymph, especially 
with reference to whether or not it originated in the leucocytes, 
could not be determined. Phagocytosis is not of decisive importance 
in connection with the destruction of anthrax infection in the hen. 
The resistance of hens against anthrax does not depend upon their 
high body temperature. 

Anthrax occurs in the ostrich as a common natural infection 
and is discussed in Chapter XVIII. 

REFERENCES 

1. Aragao. Espirochetose (treponemose) das Gallinhas. Bev. de Vet. e 
Zootech. (Eio de Janeiro), Vol. 7, 1917, p. 3. 

2. Bevan. Spirochetosis of fowls in Southern Rhodesia. /. Comp. 
Path, and Ther., Vol. 21, 1908, p. 43. 

3. Dawson. Anthrax with special reference to the production of im- 
munity. TJ. 8. Dep. Agr. Bureau Animal Indust. Bull. 13. 

A. Dubois. La fievre de Malto chez les poules. Bev. Vet., Vol. 67, 

1910, p. 490. 

5. Ehrhardt. Die Krankheiten des hansgefliigels. 3. aufl. Aarau : E. 
Wirz. 1914. 

6. Hauer. UntersuehiTngen liber die Wirkung des Mittels 606 auf die 
Hiihnerspirillose. CentralU. f. BaUeriol. {Etc.), 1 Aht. Orig., Bd. 62, 
1912, p. 477. 

7. Hindle. On the life-cycle of spirochseta gallinarum. Parasitology, 
Vol. 4, 1911, p. 463. 

8. Jowett. Fowl spirochetosis at Cape Town. Vet. Jour., Vol. 18, 

1911, p. 240. 

9. Mhrchoux et Salimbini. La spirillose des poules. Ann. de I'Inst. 
Pasteur, T. 17, 1903, p. 570. 

10. Mollhoff. Untersuchungen liber die Empfanglichkeit des Gefliigels 



SPIROCHETOSIS AND RARE INFECTIOUS DISEASES 145 

fiir Mikbrand und iiber die Grunde der Eesistenz des Huhner gegen diese 
Krankheit. Inaug. Diss. Bern. 

11. Noguchi. Cultivation of spirocliaeta gallmarum. J. hxpei. M., 

Vol. 16, 1912, p. 620. ^ T T7 ^ V ^ 7 

12. Pereira. A Espirochetose das Gallinhas. Rev. de Vet. e Zootech., 

Vol. VI, 1916, p. 327. 



CHAPTEK XIV 

LEUKEMIA AND PSEUDO LEUKEMIA 

Characterization. Leukemia in fowls is a disease of the blood, 
and blood forming organs. It is marked by changes in the com- 
p®sition of the blood manifested principally by an enormous in- 
crease in the number of leucocytes and an accompanying decrease in 
the number of erythrocytes. Besides these changes, lymphoid en- 
largement of the liver, spleen and kidneys is usually to be observed. 
Pseudo leukemia is a term desigiiating a condition in which lymph- 
oid tissue is present in the various organs, without changes in the 
circulating blood. The two conditions are very closely related, if in- 
deed they are not different stages of the same process. 

History. The disease in fowls was first recognized by Warthin 
in 1907 and soon after by Ellerman and Bang. Butterfield in 1905 
and Yutaka Kon in 1907 very likely observed cases of leukemia, 
but did not examine the blood. Pickens presents a thorough survey 
of the literature of the disease accompanied by original observations 
on a series of cases. The disease has been reported in Denmark, 
Germany and the United States. 

Etiology. Ellerman and Bang and also Yutaka Kon found pro- 
tozoa-like bodies in the organs and bone marrow of affected fowls. 
The significance of these bodies has not been definitely determined. 
In typical cases of leukemia encountered by the present writers, at- 
tempts to isolate an organism from the blood and parenchymatous 
organs have given negative results. The fact that Ellerman and 
Bang succeeded in transmitting leukemia to fowls by intravenous 
and intraperitoneal injection of a cell free filtrate of infected exu- 
dates, points to an ultra-microscopic virus as the causative agent. 

The disease is readily transmitted by non-filtered organ suspen- 
sion. The virus is present in all affected organs, but the infective 
properties of these organs are lost in a few days after death. 

There are three principal theories as to the etiology of the dis- 
ease in man which are reflected by various writers in the interpre- 
tation of lesions in the fowl: 1. The lesions of leukemia are a 
simple hyperplasia. 2. Leukemia is a neoplasm. (See lymphoma). 

3. Leukemia is a result of the multiplication of an infective agent. 

146 



LEUKEMIA AND PSEUDO LEUKEMIA 147 

Pathogenicity. Leukemia lias not been reported as occurring in 
pigeons, turkeys or guinea-fowls and experimental efforts have failed 
to produce the disease in these birds. Fowls appear insusceptible to 
subcutaneous inoculation but are infected in about 50 per cent of 
cases through intravenous or intraperitoneal injection of a suspension 
of the organs or of the blood of affected fowls. Ellerman and Bang 
observed that inoculation may produce either leukemia or pseudo 
leukemia. 

Course. The duration of the disease is variable. The period of 
incubation ranges from about 2 to 8 weeks. Death may result within 
several days after the appearance of symptoms or may be delayed 
for one to three months. Recovery is only rarely observed. 

Symptoms. While birds may die suddenly from an acute at- 
tack, the manifestations of leukemia are usually of a chronic char- 
acter. There is observed a progressive emaciation with dull, de- 
pressed appearance and noticeable weakness. In some cases the 
abdomen droops. The appetite generally remains good in the 
chronic cases but may fail in acute cases. The comb, w^attles and 
skin are pale as a result of the diminution of the red blood cells and 
increase of the white cells. Blood when drawn presents a pale red 
color and fails to clot readily, while normal fowl blood clots very 
rapidly. 

Morbid anatomy. The carcass has an anemic appearance. Us- 
ually the liver and spleen show the most marked changes. The kid- 
neys are at times also severely involved. The liver may be slightly 
enlarged, congested and sprinkled with minute whitish points, or it 
may be markedly enlarged and congested. iSTot infrequently rupture 
of the liver resulting in internal hemorrhage is observed. The en- 
larged liver may appear much darkened, soft and pulpy in more 
acute cases. In cases of longer duration, this organ is gTcatly en- 
larged and pale in appearance or else mottled and sprinkled with 
grayish white spots. It has a firm consistency and rigid contour. 
On cut section the tissue appears bloodless. The spleen generally 
shows changes in conformity with those of the liver. It may be 
only slightly congested or may be gTeatly enlarged and congested. 
As in the case of the liver, the consistency varies from soft and 
pulpy to a firm, compact mass. The color is bright mahogany in 
the case of severe congestion and sometimes grayish and brownish 
in spots. The kidneys may be several times the normal size, con- 
gested in the early stage or firm and pale at a later period. The 
intestine appears pale on the serous surface but areas of congestion 



148 DISEASES OF DOMESTICATED BIRDS 

may be present on the mucous membrane, especially in the duo- 
denum. 

Microscopically, the blood is found to contain a greatly increased 
proportion of leucocytes to red blood cells. The normal number of 
leucocytes per cubic millimeter is approximately 30,000. This is 
increased in leukemia to from 100,000 to 500,000 per cubic milli- 
meter, while the normal number of red blood corpuscles, approxi- 
mately 3,000,000 per cubic millimeter is reduced to nearly 1,000,000 
per cubic millimeter. The normal proportion of about 1 white cell 
to 100 red cells is thus changed to 1 to 2 or 1 to 3. The mononu- 
clear leucocytes increase more rapidly than the polynuclear leuco- 
cytes, or the smaller lymphocytes. Round nucleated red blood cells 
representing normoblasts and megaloblasts are to be seen in stained 
preparations. The hemoglobin content decreases from a normal 
of 50-65° to 15-20°. The blood is pale red in color and clots with 
difficulty. The liver, spleen and kidneys are found engorged with 
leucocytes. These fill the smaller capillaries and occupy a peri- 
vascular position in the parenchyma. There is a hyperplasia of the 
cells of the bone marrow and spleen, the latter being an important 
source of the leucocytes which infiltrate the liver and kidneys. De- 
generative changes are observed in the affected organs. 

Diagnosis. The presence of the disease is indicated by the an- 
emic condition of the fowl, the enlarged liver and spleen, and the 
absence of a demonstrable microorganism in these tissues. This lat- 
ter feature distinguishes it from bacterial septicemias in which the 
liver and spleen may be swollen and congested. Microscopical ex- 
amination of the blood is of the gTcatest value in differentiating from 
other affections. In simple leucocytosis accompanying infectious 
diseases, the proportion of white to red blood cells while at times ap- 
proaching 1—25 is not as striking as in infectious leukemia. Also 
the absence of myelocytes is noted in the former disease. In leu- 
kemia the white cells in the blood have approximately the following 
percentage relation : Mononuclear 70 per cent, small lymphocytes 
20 per cent and eosinophiles 6 per cent. The diagnosis of pseudo 
leukemia during life presents great difficulties. 

Treatment. As in the case of other deep seated diseases of a 
maligiiant type, treatment of individuals is unfortunately of question- 
able value. There is no definite method of treatment known which 
alters the course of the disease so as to bring about recovery. Potas- 
sium iodide in doses of 3 to 7 grams daily, and careful nursing to- 
gether with the administration of tonics, such as gentian, nux vomica 



LEUKEMIA AND PSEUDO LEUKEMIA 149 

and iron, may be of benefit in mild forms of the disease. Arsenic 
might also prove beneficial. 

Prevention. In sporadic cases of leukemia, no special precau- 
tions against the spread of the disease can be recommended other 
than the usual precaution of isolating or destroying the sick bird. 
Where several cases develop in the course of a few days, all birds 
showing the slightest abnormal appearance should be immediately 
separated from the flock. The droppings, litter, etc., should be re- 
moved and the quarters thoroughly disinfected. The drinking water 
may be medicated with permanganate of potash up to a 1-1000 so- 
lution. 

Pseudo leukemia. Ellerman and Bang regard this affection as 
being indicated by the same lesions as the true leukemia. The en- 
largement of the spleen and of the liver is often very noticeable. 
The blood is not leukemic. They consider it very probable that this 
disease has the same cause as true leukemia for cases of pseudo 
leukemia are encountered in outbreaks of the true disease. Inocu- 
lation of a hen with organs from a case of pseudo leukemia caused 
alteration of organs, typical of leukemia, with a blood picture sug~ 
gesting the beginning stage of leukemia. 

REFERENCES 

1. Pickens. Leukemia and pseudo leukemia. Rept. N. Y. State Vet. 
Co/. 1915-1916, p. 226. 

2. Ellerman u Bang. Experimentelle leukamie bei Huhnern. Ccn. 
train f. BaMeriol. (Etc.), 1 Alt. Orig., Bd. 46, 1908, S. 595. 

-3. Warthin. Leukemia of the common fowl. J. Inf. Dis., Vol. 4, 
1907, p. 309. 



CHAPTEE XV 

GENERAL DISEASES 
GOUT 

Characterization. Gout is a disease characterized by the in- 
crease of uric acid content of the blood and the deposition of uric 
acid salts in the joints as well as in various organs, especially on the 
serous membranes. The disease apj)arently does not occur in birds 
living free but is frequent in cage birds of zoological gardens and in 
all sorts of domestic birds. Among these, hens are affected most fre- 
quently, waterfowl less frequently, and pigeons least. 

Etiology. Gout appears to depend for its causation, upon the 
use of feeds rich in protein in the absence of which many breeders 
believe that it will not occur. Furthermore, a one sided diet, close 
confinement, lack of exercise and heredity appear to be predisposing 
factors. 

Two types of gout are recognized, a rare gouty arthritis and a 
more common visceral gout. 

Visceral gout. In visceral gout the serous membranes of the 
chest and abdominal cavities are covered with a layer of uric acid 
crystals of greater or less thickness. In the pericardium which is 
affected with gout with greatest frequency, there is often a deposition 
of a layer of uric acid salts 1 to 2 mm. in thickness. 

Articular gout. This type preponderates in the joints of the 
feet as well as in those of the wings. The joints are thickened and 
inflamed, while the joint capsule shows a doughy swelling. Knotty 
swellings varying in size up to that of a cherry, occur in the vicinity 
and break outwards, discharging white or grayish yellow masses 
which consist of uric acid salts. 

Hebrant and Antoine describe a case showing unusually marked 
articular lesions. The subject from which the legs were taken was 
a cock two years old. The bird otherwise appeared in good health. 
The feed had been corn and wheat. The subject could not walk for 
it was unable to stand upon the feet. 

The lesions consist of a number of tumors, some of which are as 
large as a pea. They are particularly numerous on the inferior 

150 



GENERAL DISEASES 



151 




Fig. 16. Legs of cock showing lesions of articular gout. (Drawn from plioto- 
graph by Hebrant and Antoine) 

surface of the digital region in the vicinity of the articulations. 
Because of interference with circulation the tumors have a grayish 
yellow color. Some of the tumors fluctuate and their appearance is 
suggestive of peri-articular abscesses. On incision the tumors are 
found to contain a whitish, creamy, pasty mass consisting of crystals 
of uric acid. The majority of the tumors are located in the peri- 
articular connective tissue and a small number communicate with the 
articulation. 

Gout produced experimentally. In order to determine what 
influence is exerted by protein on nutrition and the occurrence 
of gout, Kionka fed hens exclusively on horse meat that had been 
minced, and freed completely from fat. They were allowed to drink 
water as desired and soon became accustomed to the compulsory 
diet. Within a period varying from three to fifteen months they 
all became affected with gout appearing in three forms. 

In every case at first the gait became uncertain and difiicult and 
the affected birds fell often while walking. In the first type of 



152 DISEASES OF DOMESTICATED BIRDS 

the disease the pain seemed to appear suddenly and on account of 
it the bird crouched and stopped eating. This coincided with the 
appearance of isolated gouty nodules. Gradually the periods of 
pain became more frequent, the appetite was entirely lost and death 
followed. The deposits of uric acid crystals in the joints were not 
especially marked. In the second form the attacks of pain did not 
appear in so typical a manner, but the nodules were larger and oc- 
curred j3rincipally on the joint capsules and tendon sheaths of the 
wings. The third type was visceral and the deposits were limited 
principally to the serous membranes and the kidneys. The experi- 
ment proves the dietetic origin of gout. 

Diagnosis. The symptoms of the joint inflammation are dis- 
tinct: occasional loss of appetite, swelling of the joints, disinclina- 
tion to move. At other intervals, the appetite is good and the swell- 
ings decrease. At last there is no eating, inability to move, ema- 
ciation, rapid loss of strength and death. 

Visceral gout cannot be recognized in the living bird. 

Treatment. Operative treatment is of little use but may be re- 
sorted to in valuable birds. The joint tubercles should be opened 
to evacuate the contents and an antiseptic dressing applied. 

As soon as the cause of death is revealed by autopsy an appropriate 
diet should be provided for the other birds kept under similar 
conditions. The feeding of a rich proteid diet should be restricted, 
with a fast of one day a week. Grain feed, abundant gTcen feed 
or roots should be provided. 



RACHITIS 

Characterization. The disease consists of disturbance of normal 
bone formation of which the most prominent evidence is the deficient 
deposition of calcium salts. While the course of the disease is not 
well understood, it seems clear that it is caused by a general inter- 
ference with nutrition. Deficiency of intake of lime is concerned. 
Rachitis is a disease of young birds and seldom occurs in birds over 
half a year old. It is limited almost exclusively to fowls and occurs 
seldom in the turkey, waterfowl and pigeons. 

Symptoms. The birds show exhaustion, difficulty in locomo- 
tion, inappetence, diarrhea, paleness of the mucosae and emacia- 
tion. 

Morbid anatomy. Autopsy reveals intestinal catarrh and 
lesions of the bones. The large bones of the extremities are bent as 



GENEKAL DISEASES 153 

is also the breast bone which becomes S shaped. The present 
writers conducted an autopsy on a young turkey in which the 
skeleton was apparently wholly lacking in mineral constituents. The 
larger bones could be bent with the fingers and sliced with a knife. 
The bird was reported as being one of a number affected in a similar 
manner. 

Treatment. ]S[ormal feeding should be the first matter con- 
sidered. Birds should be supplied with dry, warm quarters, with 
access to grass if possible. Feed coarsely cracked grain, cracklings, 
or meat meal and burned oyster shells. Calcium phosphate may be 
administered in doses of .5 to 2.0 grams per bird, according to size. 
Small amounts of sulphate of iron may be given by putting this ma- 
terial in the drinking water in the proportion of one or two parts 
per 1000 parts of water. 'No treatment should be attempted on 
those birds liable to become cripples. Such should be killed. 

LEG WEAKNESS 

Leg weakness is a term designating unsteadiness of gait, which 
may be followed by total inability to stand on the legs. At first 
the bird otherwise appears healthy, but soon shows the effect of in- 
ability to compete with its fellows for food. If the condition con- 
stitutes paralysis, " limbemeck " may also be observed. Leg 
w^eakness also is observed in rachitis. It occurs in well fed young 
growing birds under conditions not well understood. Under such 
circumstances the ration should be reduced and green feed should 
be supplied. At other times it occurs in closely confined birds kept 
on a monotonous diet. In such cases trouble disappears when birds 
have access to the soil with consequent variety of diet. 

Polyneuritis of fowls, a condition induced by feeding polished 
rice or similar products, is the one form of leg weakness, the etiology 
of which is understood. The affection may be produced experi- 
mentally in from fifteen to twenty-five days by feeding a diet limited 
exclusively to polished rice, while a diet of natural unpolished rice 
does not produce this result. The condition of the fowl designated 
polyneuritis is generally regarded as identical with the disease of 
man called beri beri, which latter is common among people living 
almost exclusively on polished rice. It is evident that the rice hull 
contains substances, the absence of which induces neuritis. These 
have been designated vitamines. 

Vitamines of this character are not restricted to rice. It has 



154 DISEASES OF DOMESTICATED BIRDS 

been demonstrated that they are found in a large number of natural 
foodstuffs. They are very common in the seeds of plants such as 
cereals. In these, the vitamines are mainly deposited in the germ 
or embryo and to a less extent in the bran. "White wheat flour is 
deficient in vitamines and is capable of producing polyneuritis. 

The facts observed during experimentation on fowls in connection 
with the study of the etiology of beri beri of man, suggest the possi- 
bility that in isolated instances, leg weakness of chickens may be 
induced by a similar cause. 

LIMBERNECK 

Limberneck is a symptom resulting from partial or complete loss 
of control of the muscles of the neck. Probably various causes such 
as digestive disturbances, intestinal parasites and the eating of 
spoiled meat may cause this symptom. Feeding on maggots from 
decaying meat will cause limberneck. 

According to Dickson, chickens when fed botulinus toxin, become 
dull and inactive, refuse to eat, remain quiet in one place with the 
feathers ruffled. They gradually develop weakness of the legs, wings 
and neck so that they are unable to stand. The wings droop and the 
beak or the side of the head rests upon the floor of the cage. Death 
occurs within 24 hours after feeding. 

Treatment consists of administering castor oil. Preventive meas- 
ures should include precautions against allowing birds access to de- 
caying meat. 

DISEASES OF THE ALIMENTARY TRACT 
PIP 

The condition commonly termed " pip " does not represent a spe- 
cific disease, but is usually found associated with avian diphtheria. 
When the nasal passages become closed by the presence of mucous 
secretion or exudate, the fowl is compelled to breathe through the 
mouth. The constant passage of air over the tongue tends to dry 
and harden it at the tip. The dry, horny covering contracts and 
presses upon the soft tissues beneath, causing the fowl much annoy- 
ance. The hardened layer may partially separate from the soft 
tissues and expose a raw, inflamed surface. The practice among 
some poultrymen of removing the horny tip should be discouraged 
since it only increases the discomfort of the fowl by leaving a raw, 
sensitive surface exposed to foreign irritants and microorganisms. 



GENEKAL DISEASES 155 

To alleviate this condition tlie primary cause should be removed. 
An effort should be made to keep the nostrils open by removing exu- 
dates and syringing the parts with an antiseptic solution such as 3 
per cent boracic acid or 2 per cent permanganate of potash. If the 
disease which is responsible for ^' pip " is successfully treated the 
condition will disappear. 

When the symptom is noticed it is advisable to rub the tongue with 
some substance such as vaseline, cottonseed oil or glycerine. 

THKUSH 

Thrush or soor has been observed to affect the mouth and crop 
of fowls, pigeons and turkeys. The 

affection is characterized by the for- ^^^ /jl 

mation of grayish white or yellowish ^ ^nX^ Jy. // 

colored patches adhering to the mu- "^^^^ ?• °.^^^^^^c. 

ecus membrane without inflammatory ^^^^^^^^^^^^ 

changes in the latter. Severe involve- <^^^^^^ l^ ^yM\i, 

ment causes death. The organism '^^^^^^B^»^- iW^^^' 

causing the infection is designated Old- ' M^^M^^^^^^^i^l^'?/] 

iutn ( Saccliaromyces) albicans. Treat- ^^^^^^^f^lu^M 

ment of oral lesions may consist of the '^^If'^^^^^^II''^'// 

application of bichloride of mercury in // ' '^'^^^q ^ /^ 

a solution of 1 :1000. The crop may ^^^ ^^ q^^^^^^ albicans, a, cyl- 

be irrigated with boric acid solution as indrical mycelium; b, spore; c, 
in catarrh of the crop. Authoritative ^^^ ^^ '^ 
reports of the occurrence of the disease in fowls are rare. 

CATAKRH OF THE CROP 

This is a mild inflammation of the lining membrane of the crop 
due to excessive irritation by ingestion of material of an irritating 
nature, or by the products of fermentation when food for one reason 
or another, stays in the crop for an unusual length of time. It 
occurs in cases of impaction and may also be associated with certain 
infectious diseases. Parasites at times may cause the condition. 

Symptoms. The crop is usually distended with food or gas. 
The fowl appears sluggish and the appetite is diminished or lost. 
Occasionally the beak is opened wide as if to catch the breath or as 
if attempting to voinit. The head and neck also describe tossing 
movements. Later a gray, sour, ill-smelling fluid is discharged from 



156 DISEASES OF DOMESTICATED BIKDS 

the beak or from the nostrils. Without treatment the strength of the 
subject fails rapidly. 

When the disease has existed for some time in a chronic mild form 
it may assume the condition designated hanging crop. In such cases 
the musculature of the crop has been overstretched, so that after 
recovery from the catarrh, the organ does not return to its normal 
position. 

Treatment. This consists of the removal of the contents of the 
crop as soon as symptoms are noticed. If the contents are soft the 
fowl may be held head downward and the crop manipulated in such 
a manner that the material will be passed back through the esophagus 
to the mouth. This is relatively easy owing to the large diameter of 
the esophagus of fowls. Should the crop contents be hard or dry 
they may be softened by giving the bird several teaspoonfuls of water 
before attempting to remove the material. When the crop is empty, 
administer 1 teaspoonful of castor oil. Feed should be withheld for 
about 24: hours, but buttermilk, or sour milk may be freely given 
together with water. A small amount of bicarbonate of soda may 
be administered and the bird should have access to charcoal in case 
fermentation is noticeable. Fowls showing frequent attacks or 
chronic catarrh of the crop should not be retained. 

IMPACTION OF THE CROP 

Feeding with dry grains such as corn, peas, oats, or with bran 
may cause a distention of the crop. Various foreign bodies may 
cause the same condition. The enlargement of the organ will first 
attract attention. If not remedied, the condition will cause death 
of fowls in a few days, and in waterfowl in a few hours, because 
of pressure on the trachea. Massage may permit the removal of ma- 
terial through the beak, but usually incision of the crop is indicated. 

INFLAMMATION OF THE CROP IN PIGEONS 

The crop of the pigeon secretes a milk-like fluid for the nourish- 
ment of the young. If the parent birds lose their young while the 
crop is secreting this fluid, an inflammation of the crop glands 
frequently results and the organ feels hard and solid. The disease 
may be quickly remedied by substituting another squab. Only one 
should be substituted for often pigeons will not adopt two young 
ones, but kill them and throw them out of the nest. Besides, if two 



GENEEAL DISEASES 157 

were taken, the parents thus robbed of their young, would develop 
the same trouble. If such a procedure is not possible, the sick ones 
should be isolated without food. They may be allowed water slightly 
acidulated with vinegar. If abscess-like lesions occur on the breast 
they should be opened. 

GASTRITIS 

Gastritis is an inflammation of the mucous membrane of the pro- 
ventriculus or first stomach. It may result from digestive disturb- 
ances but is generally associated with the presence of strong irritants 
such as certain mineral poisons, or with infectious diseases of a 
septicemic type. Inflammation of the crop may extend to the pro- 
ventriculus. In itself, it is not of gTcat importance. 

Symptoms. The diagnosis of gastritis is difficult. If no symp- 
toms of disease are noticed other than a loss, of appetite and a slug- 
gish appearance, simple gastritis may be suspected. When associated 
with other diseases the s^nnptoms which accompany these will be 
observed. 

Treatment. The affected fowl should be given 2 teaspoonfuls of 
castor oil to which 10 drops of oil of turpentine have been added. 
Feed lightly for a time. Buttermilk or sour milk may be freely 
given. Give 30 drops of tincture of gentian twice daily. 

INDIGESTION 

Megnin distinguishes four sorts of indigestion in birds. It may 
result from lack of quality or appropriate volume of food or by 
ingestion of foreign bodies. Thus pigeons which naturally are 
granivorous will suffer if circumstances necessitate theiv consum- 
ing herbage. Birds in zoological gardens are liable to suffer from 
lack of appropriate food. Storks, herons, swans, geese and ducks 
in the winter and spring failing to obtain their natural food such as 
molluscs, slugs, etc., attempt to cheat the appetite with plants or 
aquatic mosses. These materials are to them true foreign bodies 
which cause fatal indigestion. It is the same in the case of the 
small insectivorous or semi-insectivorous birds. T\lien it is at- 
tempted to feed them exclusively on grains or vegetable mashes they 
succumb to the diet. 

Grains too large for the digestive organs of a bird act like a for- 
eign body and cause fatal indigestion. Parroquets and young pheas- 
ants may be killed in this way by grains of maize. 



158 DISEASES OF DOMESTICATED BIEDS 

Overloading the digestive organs is a second general cause of indi- 
gestion. Dry grain whicli is inviting to certain birds like the 
gallinacese is less suitable to others such as palmipeds which are ac- 
customed to soaking their food in water. Thus such birds may 
readily overload their stomachs with dry grain which may swell and 
cause death. 

Indigestion may be caused by lack of silicious gravel in the giz- 
zard. This material is indispensable to granivorous birds to tritu- 
rate the grain in that organ. Omnivorous birds likewise need grit. 
In the absence of such material, trituration is not accomplished and 
grain accumulates in the gizzard. Thus death may be caused by 
indigestion occasioned by repletion, or whole grains may pass into the 
intestine and cause a fatal inflammation. This may occur among a 
large number of birds. The present writers have observed severe 
enteritis in a wild goose occasioned by heavy snowfall and prolonged 
freezing of a pond, which circumstances prevented access to grit. In 
the absence of grit of suitable size, birds will attempt to swallow 
articles entirely too large, with fatal results. 

There is in the opinion of Megnin, an indigestion resulting from 
lack of food, or disease of hunger. Domesticated birds may acci- 
dentally be deprived of food or may be prevented from eating by 
stronger companions. 

Indigestion in birds is rarely recognized during life and is only 
encountered at autopsy. That caused by overloading may be recog- 
nized and treated with a little olive oil. Prevention along the line 
of providing suitable food and grit must be relied upon chiefly. 

INDIGESTION IN PAKKOTS 

The affection may result from a variety of causes such as improper 
feeding and failure to provide grit which impairs the natural 
function of the gizzard. The affected bird yawns, displays loss of 
appetite and occasionally manifests nervous symptoms. Correction 
of feeding is of first importance. Castor oil in a dose of from 5 to 
10 minims may be administered. Bicarbonate of soda in 5 grain 
doses may be given in the drinking water for several days, l^ux 
vomica is indicated. 

ENTERITIS 

Enteritis is an inflammation of the mucous membrane of the in- 
testine. It is perhaps the most common symptom observed in con- 
nection with poultry diseases. 



GENERAL DISEASES 159 

Etiology. Enteritis is associated with a large number of impor- 
tant diseases. It varies in the intensity of the inflammation with 
different affections. In fowl cholera, fowl plagiie and several other 
septicemias the inflammation is very severe, while in fowl typhoid 
and infectious leukemia the mucous membrane may show little or no 
congestion. Enteritis is associated with such protozoal diseases as 
coccidiosis and infectious entero-hepatitis, and with intestinal worm 
infestation. 

Mineral poisons may set up an inflammatory condition, as may 
also moldy or putrid food. 

In birds deprived of grit, the food passes from the gizzard with- 
out being triturated and causes severe enteritis with hemorrhage into 
the lumen of the intestine. 

Symptoms. The most prominent symptom of enteritis is diar- 
rhea. The droppings may be watery or semi-solid. The color 
varies according to the particular disease which is present. It may 
be white, brownish, gTeenish, yellowish or mixed in color. The fowl 
displays a loss of appetite in the more severe forms of enteritis, be- 
comes droopy, weak and somnolent. Paralysis of the legs frequently 
occurs in connection with inflammations of the intestine. Unusual 
thirst is often in evidence. 

Treatment. As enteritis is usually associated with some more 
important disease, the disease should be properly diagnosed and 
treated. Simple enteritis due to minor causes may be treated by re- 
moving the irritating substances from the intestinal tract by means 
of a purgative such as castor oil in 2 teaspoonful doses or Epsom salts 
in Ys to ^2 teaspoonful doses, A tonic consisting of powdered gentian 
1 dram, powdered ginger 1 dram and powdered sulphate of iron 15 
grains may be given. Mix /4 teaspoonful in the feed twice daily. 
The water for the entire flock may be made antiseptic by the addition 
of % oz. of carbolic acid to the gallon of water. This will tend to 
prevent the spread of infection to others of the flock in the event that 
the affected bird or birds are harboring an infectious disease. The 
carbolic acid treatment may be discontinued after a few days in the 
event that no more fowls are attacked. 

SIMPLE DIARRHEA 

Fowls are sometimes affected by a diarrhea which is not appar- 
ently associated with one of the more important diseases. A watery 
or semi-fluid discharge may result from an irritation or derangement 



160 DISEASES OF DOMESTICATED BIRDS 

of the intestine independent of the action of infectious organisms. 
Among the causes which may produce a catarrhal condition of the 
intestinal mucous membrane and result in simple diarrhea are diges- 
tive disturbances of an obscure nature, sudden changes in the feed 
or an unusually large supply of green feed, too much meat scrap, 
especially irritating substances in the feed, moldy grains or decom- 
posed flesh. Mineral or other irritants which are not taken in suf- 
ficient quantity to cause poisoning or enteritis may produce a simple 
diarrhea. Fermentation of the contents of the intestine may result 
in diarrhea. 

Treatment. The cause of simple diarrhea being direct intestinal 
irritation, the obvious remedy is to remove the cause. Where only a 
few birds are affected they should be given 2 teaspoonfuls of castor 
oil each. The entire flock may be given Epsom salts if necessary, 
in the proportion of Vs to Y2. teaspoonful to each grown fowl. The 
salts may be dissolved in water and mixed in a mash to be fed early 
in the morning. If suspicion points to the feed as the cause of diar- 
rhea it should be changed or fed in smaller amounts combined with 
other feeds. 



CONSTIPATION 

This is apparently not a common ailment of fowls. It does, how- 
ever, occur to some extent in fowls confined in small quarters for 
long periods with insufficient exercise. Lack of green or succulent 
feed also tends toward constipation. Following diarrhea there may 
be a temporary or slight constipation. The condition in young chicks 
suffering from white diarrhea known as " pasting up behind " can- 
not be considered a true constipation since the droppings are merely 
held back by the drying of the discharges in the do^vn surrounding the 
vent. Fowls allowed free range, or large runs and properly fed are 
practically free of constipation. 

Treatment. The condition may be relieved by administering 
substances which will cause an increased secretion of fluid from the 
intestinal mucosa, or increased peristalsis. Two teaspoonfuls of 
castor oil or Ys to Y teaspoonful of Epsom salts to each affected bird 
would be indicated. 

Gage and Opperman have determined the dosage of Epsom salts for 
birds of various ages as follows : 



GENERAL DISEASES 161 

Age Dose 

1 to 5 weeks 10 grains 

5 to 10 weeks 15 grains 

10 to 15 weeks 20 grains 

15 weeks to 6 months 30 grains 

1 year and over 40 to 45 grains 

To facilitate figuring quickly the number of ounces required for 
treating a number of birds they furnish the following information 
concerning equivalent weights: 

1 pound avoirdupois equals 7000 grains. 

1 ounce avoirdupois equals 437.5 grains. 

1 pound Troy or apothecary equals 5,760 grains. 

1 ounce Troy or apothecary equals 480 grains. 

The constipation may be due to obstruction by foreign bodies, to 
worms in the intestines, or to matting of feathers over the cloaca. In 
the latter condition, softening of the mass and removal of the obstruc- 
tion is first in order. After removal of the material in the cloaca, 
rectal injections of soapy water or olive oil may be made. In very 
small birds a probe wet with glycerine or castor oil may be in- 
serted in the rectum. 



DISTENTION OF THE BURSA OF FABRICUS 

Occasionally the bursa of Fabricus may become enormously dis- 
tended into a cyst-like structure containing a clear, colorless fluid. 
Schantyr has observed two cases in which the fluid amounted to over 
700 c.c. He observes that when an exploratory puncture is made 
in case of distention of the abdomen with fluid, a yellowish fluid in- 
dicates ascites, while a colorless fluid indicates hydrops of the bursa 
of Fabricus. 



DISORDERS OF THE LIVER 

Disorders of the liver such as enlargement, fatty degeneration, 
jaundice and the occurrence of various sorts of diseased areas in 
the organ cannot be classified as separate entities. In most cases, 
livei' lesions merely consist of a portion of the lesions characteristic 
of the common infectious diseases. Various septicemias, tuber- 
culosis, ontero-hepatitis, leukemia and tumors may display more or 
loss characteristic lesions in the liver. Perhaps under some condi- 
tions hypertrophy or enlargement of the organ may be due to heavy 



162 DISEASES OF DOMESTICATED BIEDS 

feeding undej 
in the winter. 



feeding under close confinement as occurs among fowls fed on com 



DISEASES OF THE RESPIRATORY TRACT 
BRONCHITIS 

Fowls are quite frequently affected by a catarrhal inflammation of 
the mucous membrane lining the air passages of the throat and lungs. 
This condition usually results from the extension of inflammation 
from the mouth and nasal chambers. Often birds which have recov- 
ered from avian diphtheria are observed to be affected with bron- 
chitis. This may persist for a short time or become chronic. 

Symptoms. In severe cases the fowl displays a marked difficulty 
in breathing. The neck is more or less straightened out to facilitate 
the passage of air. The breathing is noisy and the fowl may gasp 
in a manner similar to that shown by a chicken affected with gapes. 
The beak may be kept open, and a mucous discharge is given off 
through the mouth. The bird is observed to make efforts to dislodge 
this discharge by shaking the head. 

In less severe or chronic bronchitis the symptoms are not so notice- 
able. There may be only slight difficulty in breathing, accompanied 
by a wheezing sound. The mucous membrane of the bronchi and 
trachea becomes thickened and may show patches of yellowish exu- 
date especially in the two large bronchi. 

Treatment. Since bronchitis is often attributed to exposure to 
cold draughts and dampness these conditions should be corrected. 
Affected birds should be placed in warm quarters, free from air cur- 
rents. Under good hygienic surroundings the attack may pass off 
in a short time. In acute cases the administration of 5 drops of 
wine of ipecac is beneficial. In chronic bronchitis treatment is not 
satisfactory. 

CONGESTION OF THE LUNGS 

The lungs may become congested as a result of the extension of 
an inflammation from the larger bronchi into the minute air tubes 
and air sacs. The congestion is generally of an acute type. It may 
be induced by the fowl becoming wet and severely chilled. In the 
early stages of pneumonia congestion of the lungs is the most marked 
symptom. 

Symptoms. Simple congestion is differentiated from pneumonia 
on post mortem examination by the bright red appearance of the 



GENEEAL DISEASES 163 

lungs in the former and by the fact that pneumonic lungs are hepa- 
tized and will sink when placed in water. Affected birds show a 
distressed appearance and breathe with difficulty. The respirations 
are short and panting. The discharge and wheezing observed in 
bronchitis are absent. The normal temperature of 107° to 108° F. 
is raised 2 or 3 degrees. The birds have an increased thirst. Evi- 
dence of pain is produced by pressure on the ribs over the lung area. 

Wher-e both lungs are affected death may follow shortly after the 
onset through pressure on the air cells resulting in a shutting off of 
the air supply and suffocation. In less severe cases the congestion 
may subside or the condition may develop into pneumonia. 

Treatment. The bird should be placed in warm quarters and 
given a diet consisting largely of green food. One third to one half 
teaspoonful of Epsom salts dissolved in water should be administered 
once a day for two or three days. Also give 10 drops of spirits of 
nitre twice daily. 

PNEUMONIA 

Characterization. Pneumonia of fowls is of relatively rare oc- 
currence in the classic form distinctive of this disease in other ani- 
mals. The disease is sporadic in character and frequently only one 
bird in a large flock may be infected. 

Etiology. Pure pneumonia cases which have come under the 
observation of Gallagher have been due to the presence of the 
pneumococcus. It has the characteristic diplococous form on micro- 
scopic examination and is similar in its cultural characteristics to 
the pneumococcus of Frankel. Its infrequent sporadic invasion sug- 
gests that the fowl is normally resistant, and that predisposing causes 
of an obscure nature are responsible for its pathogenicity in certain 
individuals. 

Symptoms. The most characteristic symptoms are more rapid 
breathing with physical signs of distress and general malaise. 
There may be a mucous discharge from the nostrils, and the tempera- 
ture is elevated. As the disease progresses, the comb assumes a 
darker color at the tips, or rear, or in hanging combs at the more 
dependent portions. This darkened appearance progresses with the 
disease and practically the entire comb may assume a purplish color 
due to lack of oxygen in the circulating blood and weakened heart 
action. In fatal attacks, the strength fails rapidly and the bird 
reaches a comatose condition in which it may linger for several hours 
before death. 



164 DISEASES OF DOMESTICATED BIRDS 

Morbid anatomy. In the normal fowl, on post-mortem examina- 
tion, the lungs are found deflated, fairly compact and closely applied 
to the ribs. They occupy less volume relatively, than is the case in 
other animals. This is, no doubt, due to the peculiar respiratory 
system of birds which has, in addition to the lungs, a number of air 
sacs in the pleural and abdominal cavities, and also air canals in 
the larger bones. In a pneumonic condition the lungs are distended, 
darkened and solidified to a greater or less degree, approaching the 
condition known as red hepatization or liver consistency. They will 
sink in water, while normal or simply congested lungs will float. 
The pneumonic lung stands out in a firm position surrounding the 
heart and may be found adhering to the pericardial sac. There are 
usually no visible areas of necrosis, but the bronchioles and larger air 
tubes are filled with an emphysematous mucous discharge. 

Treatment. Owing to the fact that pneumonia is induced by the 
presence of organisms in the lung tissues, and that these cannot be 
reached by disinfectants which would not destroy the sensitive mem- 
branes of the air cells, treatment has been found futile in most cases. 
During the early stages, or in milder cases, stimulants such as strych- 
nine in doses of %o to Vso gr., or 50 per cent alcohol in quantities 
of H dram may be given by way of the mouth. Because of the 
dense breast muscles, local external applications are not indicated. 
The patient should be placed in quarters where the temperature ap- 
proximates 70° F. and soft mashes, or sweet or buttermilk given as 
a food. Since the disease is sporadic in a flock, no special prevent- 
ive measures are necessary to guard against its spread. 

DISEASES OF THE OVIDUCT 
INFLAMMATION OF THE OVIDUCT 

The oviduct may be highly congested or inflamed as a result of the 
condition known as " egg bound," prolapse, or the presence of ac- 
cumulated egg material which has been arrested by a tumor forma- 
tion in the wall of the oviduct. Organisms which gain access to 
the oviduct find a favorable medium for development in such ma- 
terial. They give rise to decomposition products which irritate the 
mucosa of the organ and set up an inflammatory condition. Broken 
eggs in the oviduct or excessive effort in laying may lead to inflam- 
mation. The oviduct may become affected through the spread of 
inflammation from the ovary or other adjacent organ or it may be 
involved with other organs in certain generalized diseases. 



GENEKAL DISEASES 165 

Symptoms. Where the inflammation is confined to the oviduct 
no general change in the appearance may be apparent except in 
severe cases. A tendency of the fowl to make efforts to lay at fre- 
quent intervals is often noticed. Eggs w^hich are abnormal either 
in their structure or form may be passed. These may be blood 
stained. Most frequently the eggs are small and contain only al- 
bumin. Shell-less eggs are also laid. In fatal cases the fowl ex- 
hibits symptoms of general debility, with loss of appetite, pale comb 
and leg paralysis. 

Treatment. When symptoms are apparent an effort should be 
made to locate the cause of the trouble. Manipulation with the 
finger through the cloaca or over the abdominal wall may disclose the 
presence of an obstructed egg, broken egg or egg concretion which 
may be removed after the manner described for the treatment of 
" egg bound." The fowl should be isolated, given green food, soft 
mashes and /4 teaspoonful of Epsom salts. 

RUPTURE OF THE OVIDUCT 

In severe inflammation of the oviduct when a large mass of egg 
concretion is present, or an attempt to pass an egg of large size is 
made, the wall of the oviduct may be split allowing the mass or egg 
to pass into the peritoneal cavity. Other eggs or egg material 
may follow through the opening and accumulate in the cavity. 
These later induce peritonitis, or the rupture may heal and the ovi- 
duct continue its normal activities. 

The condition would be suspected by the sudden suspension of 
laying accompanied in many cases by a rapid increase in the size of 
the abdomen. Manipulation would disclose the presence of abdomi- 
nal egg concretions or accumulated eggs. 

Rupture of the oviduct is of comparatively rare occurrence. 
Treatment if advisable would be by surgical means. 

EGG BOUND 

This condition is of frequent occurrence in fowls, especially in 
young pullets. It represents an inability on the part of the bird to 
pass the egg in the normal manner from the oviduct, or cloaca. 
This failure may be due to an inflammatory condition, stricture, or 
tumor formation in the posterior portion of the oviduct, or cloaca, 
or to prolapse of the oviduct. In pullets which are beginning to 
lay, however, the usual cause is the undeveloped state of the egg 



166 DISEASES OF DOMESTICATED BIRDS 

passage which has not jet become sufficiently dilated to accommodate 
eggs of large size. Mature hens may become egg bound through at- 
tempts to pass malformed, or double yolked eggs. It is generally 
noted that the first eggs of the pullet are elongated and of smaller 
diameter than those delivered after laying has become well estab- 
lished. Also the first eggs frequently show streaks of blood indicating 
the difiieult passage through the last portion of the oviduct or through 
the vent. Cross breeding which unites a breed of large egg type with 
one of a smaller egg; type would be conducive to the formation of a 
large egg for which the egg passage might not be developed in 
proportion. 

Symptoms. The affected hen is observed to be restless, leaving 
the others and going frequently to the nest to make attempts to lay. 
The effort after a time results in an inflamed condition of the oviduct 
and cloaca. The condition often results in an eversion or prolapse of 
these organs. The distress of the fowl and the extruded, inflamed 
parts may attract other fowls. These begin to pick at the mem- 
branes and if the victim is not rescued in time a large portion of the 
intestine may be torn away and dragged through the vent causing 
the death of the bird. Where prolapse has not occurred the affected 
fowl may continue to make an effort to lay the egg until successful 
or overcome by weakness. 

Diagnosis. The presence of an egg in the oviduct may be de- 
termined by palpation of the posterior abdomen or exploration 
through the vent. 

Treatment. Several methods of treatment are practiced. The 
fowl may be held vent downward over steaming water for a time 
and then placed upon the nest. The steam has a tendency to relax 
the parts and make easier the voiding of the egg. Lubricating the 
vent and cloaca with sweet or linseed oil may also aid the fowl in 
mild cases of egg bound. However, the quickest and surest method 
is the removal of the egg by the following procedure. The hen is 
held by an assistant with her back downward, while the operator 
passes the forefinger through the vent and pushes aside the mem- 
branes until the egg shell is felt. With the fingers of the other hand 
pressing on the external wall of the abdomen the egg is forced toward 
the vent, being guided along the inflamed membranes of the egg 
passage by the inserted finger. When the shell is visible through the 
vent it is punctured by means of a sharp pointed instrument such 
as a knife or awl. It is broken into small pieces with a pair of 
forceps or with the finger and is removed with its contents. The 



GENEEAL DISEASES 167 

patient should be isolated and the inflammation reduced by fre- 
quent injections of cold or ice water into the cloaca. 

Fowls which have sutiered from egg bound due to the presence of 
a large egg or to tardy development of the egg passage are not perma- 
nently alfected. Egg bound due to pathologic alterations in the 
oviduct is not open to practical treatment. 

PROLAPSE OF THE OVIDUCT 

Eversion of the oviduct is usually associated with difficulty in lay- 
ing as in the condition known as '' egg bound." The mucosa of 
the extruded cloaca and oviduct becomes highly congested. The pro- 
lapsed organs are observed as a dark red or purplish mass projecting 
through the vent. The affected fowl is soon noticed by the others of 
the flock and if it is not rescued in time it will be attacked and de- 
stroyed as a result of the pi-otruding tissue being torn away and 
devoured. 

As soon as the bird is discovered it should be placed by itself and 
carefully treated. The oviduct should be explored with the finger, 
which should be greased or oiled, to locate an egg or other cause. If 
an egg is present it may be removed as described for " egg bound." 
The prolapsed tissue is carefully returned through the vent, after 
which cold water is injected to reduce the congestion and promote 
the contraction of the oviduct wall. This may be continued for 
some time or repeated at frequent intervals until a cure has been 
effected. 

VENT GLEET 

Characterization. Vent gleet or cloacitis is an inflammatory 
disease of the vent and cloaca of fowls. It appears to be spread en- 
tirely by coitus and may be considered an infectious venereal disease. 
Its causative agent has not been determined. 

Symptoms. In the early stages of the disease there is a conges- 
tion of the membrane of the posterior portion of the cloaca and mar- 
gin of the vent. This may extend to the lower portion of the oviduct 
and rectum. The fowl exhibits signs of severe irritation, frequently 
voiding small droppings. A watery discharge which later becomes 
purulent and foul smelling is passed out through the vent. The skin 
around the vent becomes swollen and reddened and an offensive odor 
is usually present. The irritation causes the fowl to peck at the 
part. Other fowls may be attracted by the discharge, and the red- 
dened appearance of the affected region and may peck at the skin 



168 DISEASES OF DOMESTICATED BIKDS 

causing an ulceration of the surface. Frequently the diseased fowl 
dies as a result of the tearing of the cloaca and rectum by its canni- 
balistic mates. The presence of the disease in a flock causes a 
marked falling off in the egg yield and a decrease in the fertility of 
the eggs. 

Treatment. Vent gleet is very resistant to treatment. It is 
usually better to destroy the diseased bird than to attempt treatment. 
This is especially so in the case of the first birds attacked as by this 
means its spread may be prevented. Where treatment is desired the 
affected birds should be isolated. The discharge may be removed 
from the skin and feathers by washing with warm water. Anti- 
septics such as 5 per cent carbolic acid, or 1-1000 corrosive sublimate 
are to be applied to the external affected area, or a 2 per cent car- 
bolic ointment may be rubbed over the part. Argyrol in 15 per cent 
solution or cresol in 2 per cent solution may be injected into the 
cloaca twice daily. Roosters should be removed from the flock 
Mdiile the disease is present and if any are found diseased it would be 
advisable to destroy them. 

STRUCTURE OF THE FECUNDATED EGG OF THE FOWL 

The ovum or yolk on its release from the ovary and entrance to the 
oviduct appears as a yellowish ellipsoid body about one inch in diame- 



Fio. 18. 1, air sac; 2, shell; 3, white yolk; 4, blastoderm; 5, yellow yolk; 6, 
dense albumin; 7, chalaziferous layer of albumin; 8, fluid albumin; 9, 
chalaza; 10, shell membrane. (Original) 

ter. It is somewhat flattened on one surface, which presents an 
opaque whitish circular spot, the germinal disc (Fig. 18). Cell 



GENEKAL DISEASES 169 

multiplication is already taking place in this disc, from whicli the 
embryo develops. The yolk is composed of a central light colored 
portion (Fig. 18) and an outer mass colored a deeper yellow. The 
latter is formed of concentric layers showing different stages of yolk 
deposit (Fig. 18). The germinal disc and yolk are surrounded by 
a thin strong vitelline membrane (Fig. 18). The ovarian ovum on 
entering the oviduct is passed along by peristaltic movement in a 
rotary course to its completion in the uterus or shell secreting por- 
tion. In the anterior portion of the oviduct the membrane chal- 
azifera is applied over the vitelline membrane. It consists of a 
dense layer of albumin and gives rise to the two chalazse which ex- 
tend from each pole of the ovum. These strands become twisted in 
opposite direction during the further passage of the ovum through 
the oviduct. Over the chalaziferous membrane are several albumi- 
nous layers secreted by the glands of the oviduct. When the ovum 
enters the isthmus or narrow portion two egg membranes are secreted. 
These become separated at the large end of the egg as air is absorbed. 
The shell is acquired in the uterus. 

FOREIGN BODIES IN EGGS 

Eggs may contain a variety of foreign bodies such as pebbles, frag- 
ments of plants, feathers, roundworms, etc. Such bodies after gain- 
ing access to the cloaca penetrate the oviduct far enough to encounter 
an egg and thus be included within the shell. 

Otherwise normal eggs have been found to contain such parasites 
as the fluke Prosthogonimus ovatus and the roundworm Ascaridia 
perspi^cillum. The latter worm may be present surrounded by al- 
bumin in an abnormal egg lacking a yolk. It is apparent that under 
such circumstances the presence of the worm has stimulated the secre- 
tion of the albumin. Tapeworms and segments of the same have been 
found in eggs. The parasites found in eggs evidently have migi-ated 
into the oviduct for a sufficient distance to meet a developing egg and 
to become enclosed in shell. Parasites of microscopic size such as 
coccidia, amebse, aspergillus fungi and bacteria have been demon- 
strated in eggs. 

BLOOD SPOTS IN EGGS. (lIVER SPOTs) 

It frequently happens that streaks of blood, or clots of varying size 
are found in eggs. This abnormality is especially noticed during the 
heavy laying period. At such time the ovary is plentifully supplied 



170 DISEASES OF DOMESTICATED BIRDS 

with blood to promote the rapid formation of ova. As an ovarian 
follicle ruptures to release an ovum some blood may escape from a 
congested blood vessel of the follicle. The blood passes into the 
oviduct along with the ovum where it becomes surrounded by al- 
bumin and is incorporated in the egg. The size of the spot or clot 
depends upon the amount of blood which has escaped. These clots 
are often taken for pieces of flesh and are commonly referred to as 
liver or meat spots. The wholesomeness of such an egg is not im- 
paired. There is no practicable means known for preventing the 
occurrence of blood spots in eggs. However by candling the entire 
product of a flock, it is possible to prevent such eggs from going on 
the market. 

DISCOLORED YOLKS 

N^ewly laid eggs in some instances exhibit a darkened appearance 
of the yolk which is not due to developmental changes in the ovum or 
to decomposition as a result of bacterial action. The entire yolk 
may appear dark in color or the discoloration may be confined to 
spots or streaks on the surface or in the depths of the yolk material. 
In testing for freshness by candling or on opening the egg, such a 
discoloration may be mistaken for an evidence of addling. The con- 
dition results apparently from the action of sulphur, normally pres- 
ent in the yolk, on small globules of cottonseed oil which are absorbed 
into the yolk. This occurs when the fowls are being fed cottonseed 
meal or material containing cottonseed oil. This oil may be present 
in table scraps since it is often an ingredient of butter, oleomar- 
garin or cooking oils. Cattle or hog fats or their products may 
contain cotton seed oil where the animals have been fed cotton 
seed meal shortly before slaughter. 

Yolk is composed of albumin 17.50 per cent, oil and salts 28.75 
per cent, and water 53.75 per cent. The yolk granules are ar- 
ranged in thin concentric layers as they are received through the 
surrounding vitelline membrane from the blood vessels in the ovarian 
capsule or follicle. This arrangement would explain the disposi- 
tion of the discoloration, depending on whether the fowl was re- 
ceiving cottonseed oil constantly or only at intervals. The color 
reaction between sulphur and cottonseed oil is utilized in the 
Halphen test for the presence of the latter as an adulterant in 
certain food products. In a positive test a pink color is produced 
but this is changed in the yolk to a brownish or dark yellowish color. 
It is not improbable that discolored yolks may result also from the 



GENEKAL DISEASES 171 

action of the contained sulphur on certain metallic salts which the 
fowl may ingest and which through metabolism may be incorporated 
into a yolk. 

There is no apparent reason why eggs so affected should be un- 
wholesome. They may be detected by candling. 

DOUBLE YOLKED EGGS 

The inclusion of two yolks within one shell is due to rapid 
ovulation or delay of one yolk in its progress to the isthmus or egg 
membrane-secreting part of the oviduct, thus allowing the following 
yolk to reach it and be surrounded by a common membrane. When 
the two yolks do not meet until arrival at the isthmus, each is sur- 
rounded by a separate layer of albumin. When two yolks are ovu- 
lated within a short interval or meet in the anterior portion of the 
oviduct they may have a common layer of albumin and common 
membranes. 

SOFT SHELLED EGGS 

When the egg reaches the uterine portion of the oviduct under 
normal conditions the double membrane secreted by the isthmus 
is covered by a felty fibrous layer into which is deposited the ma- 
terial which forms the calcareous shell. Absence of the hard shell 
may be due to several causes. If the bird does not have feed con- 
taining lime salts in sufficient quantity, or access to substances rich 
in these salts it is apparent that a normal shell cannot be produced. 
Providing the fowls with crushed oyster shells or mortar will remedy 
this defect. Irritation of the oviduct as a result of inflammation 
may cause an abortion of the egg before it is properly formed. 
Sudden fright may also lead to a premature laying of the egg before 
it has acquired its hard shell. Excessive attention by the male is 
said to cause the laying of soft-shelled eggs. Where this is con- 
sidered as the cause the removal of the cock is indicated. Except 
when eggs are desired for incubation the presence of a male bird in 
the flock is not necessary since fowls lay equally well or better in his 
absence. Unfertilized eggs keep better than fertilized ones, a fact 
which causes many poultry men to place cock birds in the flock 
during the breeding season ©nly. 



172 DISEASES OF DOMESTICATED BIEDS 



DISEASES OF THE PERITONEAL CAVITY 
ABDOMINAL YOLK CONCKETIONS 

The presence of masses of yolk material lying free in the peri- 
toneal cavity of hens is frequently observed on post-mortem ex- 
amination. The cause of this condition is not always apparent. 
Injuries to the membrane of the fallopian tube, or tumor forma- 
tions in the oviduct which interfere with the entrance of the yolk 
or its passage through the oviduct are usually responsible. Yolks 
or partly formed eggs may be returned through the oviduct and 
aborted into the peritoneal cavity by reverse peristalsis induced by 
inflammatory changes in the wall of the oviduct. At times the 
contents of only one yolk or ovum may be present while in other 
cases the concentric layers of yolk substance indicate that the process 
has been going on for a considerable period of time. In the latter 
instance the mass may be as large as a tennis or base ball and of 
firm consistency. The layers are easily separated when newly 
formed or before organization or decomposition changes have pro- 
gressed. Some accumulations reveal a center of albumin, or par- 
tially formed shell membrane, while others exhibit a yolk formation 
throughout. Occasionally a normal yolk is found surrounded by 
a small amount of albumin and inclosed in a soft or partially cal- 
cified membrane. In this case there is evidence that the ovum 
has passed into the oviduct and owing to an abnormal state of this 
organ, reverse peristalsis has caused its return through the fallo- 
pian membrane into the abdominal cavity. Quite frequently as 
many as five to seven perfectly formed yolks in a good state of 
preservation are found between the intestinal convolutions. These 
apparently represent a recent discharge from the ovary in contrast 
to the solidified yolk substance constituting the typical yolk con- 
cretion. 

Symptoms. The presence of yolk deposits is not disclosed by 
external appearances where putrefactive changes are absent. The 
tendency is for the material to become partially absorbed. The un- 
absorbed portion is formed into a rounded body which increases in 
size according to the number of ova aborted into the cavity. In the 
event that organisms find their way into the peritoneal cavity, pre- 
sumably by way of the oviduct, a favorable culture medium is at 
hand and decomposition changes may be inaugurated which lead to a 
septic condition and result in peritonitis, or septicemia. 



GENEEAL DISEASES 173 

Treatment. The removal of the yolk masses is easily accom- 
plished by an incision through the abdominal wall once the nature 
of the affection has been determined by digital exploration. As a 
rule the presence of aborted egg material is not suspected during the 
life of the fowl and treatment is therefore not practiced. It is also 
apparent that treatment to be effective would require the correction 
of the factors which lead to the misplacement of the ova. The ob- 
scure nature of these renders attempts at their control impractical. 

DROOPING ABDOMEN 

In the heavy breeds, especially, the abdomen may show a tend- 
ency to assume a pendant position, frequently coming into contact 
with the ground when the bird is in a standing position. The skin 
of the abdomen may be devoid of feathers, and usually shows a 
reddened appearance. This is often due to a marked accumulation 
of fat in the abdominal wall and visceral organs. More often it 
results from a displacement of the gizzard. This organ, owing to an 
elongation of the proventriculus or true stomach, is carried back- 
ward and instead of resting in its normal position on the posterior 
floor of the sternum, takes up a position on the much less resistant 
membranous wall of the abdomen. As a result of its weight and 
muscular activity in a cavity already overfilled with distended in- 
testines and accumulated fat it forces the inferior abdominal wall 
into a drooping or dragging position. The abnormal position of the 
gizzard may be detected by palpation of the parts immediately 
behind the sternum where the outline of the dense muscular organ 
can easily be followed. 

Treatment consists of the restriction of fat forming foods in 
the diet. It is inadvisable to use birds showing this condition for 
breeding purposes, since the evident tendency to lack of tone and 
resistance in the parts concerned would be perpetuated to a greater 
or less extent in the progeny. 

ASCITES (dEOPSY) 

Characterization. This condition consists of an accumulation 
of fluid in the peritoneal cavity or abdomen. 

Etiology. 'No one specific causative agent is responsible. The 
accumulation of fluid results from a filtration of blood serum 
through the serous membranes of the intestine, or the peritoneal 
covering of the abdominal cavity or paryenchymatous organs. It 



174 DISEASES OF DOMESTICATED BIRDS 

may be present in severe, or chronic cases of enteritis, sarcomatosis, 
tuberculosis, peritonitis or other debilitating diseases affecting the 
abdominal organs. 

Symptoms. Except in a marked dropsical condition, no external 
manifestations of ascites are readily noticeable. On palpation of 
the abdominal region the presence of fluid may be detected. Its 
presence has no great diagnostic importance since it is merely as- 
sociated with a more serious affection which may be difficult of ac- 
curate determination during the life of the bird and which in the 
large percentage of cases is not open to practical treatment. 

Differential diagnosis. Ascites is often confused with an ex- 
cessive formation of fat in the abdominal wall or with a drooping 
abdomen. Palpation of the abdomen and the absence of emaciation 
or other signs of disease would eliminate ascites. When the latter 
is present a distinct fluctuation of liquid is felt, much the same as 
in the palpation of a water bag. 

Treatment. When detected, the fluid may be evacuated by punc- 
ture of the abdominal wall with a hypodermic needle. Except in 
cases of septic ascites this method of procedure would be of little 
permanent value since the fluid would be readily absorbed in the 
event that the primary cause of its presence were corrected. 

PEEITONITIS 

Characterization. Peritonitis occurs frequently in domesticated 
birds. It is manifested by an inflammatory condition of the serous 
coverings of the visceral organs accompanied by a serous, or coagu- 
lated exudate in the peritoneal cavity. 

Etiology. Various causes may be responsible for this affection. 
There are numerous specific diseases of a septicemic nature in which 
the involvement of the peritoneum is of secondary consideration. 
Besides these the most important direct causes of peritonitis are 
infected yolk concretions or deposits, ovarian infections, extension 
of inflammation of the oviduct, or rectum, as a result of rupture, 
perforation of the digestive tract by foreign bodies or as a result of 
ulcerative changes in the intestinal wall such as sometimes occur in 
coccidiosis of fowls, or entero-hepatitis of turkeys. 

Symptoms. These are nonspecific since the general attitude of 
an affected bird is similar to that displayed in several other in- 
fectious diseases. Diagnosis is difficult except through post-mortem 
examination. The disease is usually of an acute nature, death 



GENERAL DISEASES 175 

resulting- sliortly after the appearance of symptoms. The affected 
fowl shows loss of appetite, ruffled feathers, elevation of temperature, 
weakness and extreme dc])ressi(m. Diarrhea is frequently observed 
especially when the intestinal serosa is extensively involved. In 
cases of peritonitis due to rupture of the rectum, the droppings are 
scanty owing to the passage of a portion of the intestinal contents 
into the peritoneal cavity. The presence of yolk concretions, or 
fluid in the abdominal cavity may assist in a diagnosis. In either 
case the abdomen may show a pendant position. On palpation, the 
fluctuation of liquid may be felt, while the presence of concretions 
is determined by their dense consistency, free disposition and rounded 
contour. 

Morbid anatomy. The pathologic picture in peritonitis in birds 
is not usually marked by extensive congestion of the serous lining of 
the abdominal cavity and visceral organs. There may be localized 
areas of congestion, or hemorrhagic spots on the visceral peritoneum, 
especially that covering the ovary. In the majority of cases no 
macroscopic evidence of congestion is apparent. The disease is more 
often marked by exudates either of a serous, or semi-solid form. 
Evidently the morbid condition results principally from the absorp- 
tion of toxins generated by the action of microorganisms on foreign 
matter which has gained entrance to the cavity. The serous exudate 
is at times clear and straw colored, at other times cloudy and putrid. 
The septic condition is generally associated with a cheesy exudate 
which covers the viscera in small masses and is non-adherent to the 
membrane. Yolk concretions, or individual aborted yolks, display 
putrefactive changes. Where rupture of the oviduct or intestine has 
occurred, egg material or intestinal contents respectively will be 
found and the rupture may be easily located. 

Treatment. The difficulty in diagnosing peritonitis during the 
life of the bird and the advanced stage reached when symptoms be- 
come apparent renders attempts at treatment impractical. Should a 
physical examination reveal the presence of yolk masses free in the 
abdominal cavity, or a dropsical condition of the abdomen, surgical 
methods could be employed to remove the accumulations. The cavity 
could then be washed with sterile water or a mild antiseptic to remove 
septic exudates. 

VICIOUS HABITS 

Toe pecking. The conditions surrounding incubator chicks kept 
together in large numbers in brooders, are very different from those 



176 DISEASES OF DOMESTICATED BIRDS 

afforded a brood of chicks under the care of a hen. One of the most 
troublesome results is the habit of pecking toes. Anything unusual 
about the foot of a chick attracts the attention of another member 
of the flock which pecks at the foot. The attention of others is drawn 
to the action and they repeat the pecking. As soon as blood is 
drawn, the deep seated instinct of chickens to attack the injured 
or the weakling, is aroused and the victim is soon killed or seriously 
maimed. The habit is likewise manifested by pecking at the vent. 
In this way a chicken is disembowled in a surprisingly short length 
of time. Once the taste for blood is aroused, the chicks attack one 
another indiscriminately and cause heavy losses. 

The immediate remedy is to remove instantly all wounded birds, 
which must be kept in isolation until entirely recovered. General 
precautionary measures will include those designed to keep the chicks 
occupied with harmless pursuits. Various kinds of food hung so as 
to be somewhat inaccessible, furnish diversion. Dried meat has 
been so employed. 

Egg eating. The habit of eating eggs is often established by 
the accidental breaking of an egg. The practice spreads rapidly by 
imitation. Careful observation will reveal yolk stains on the beaks 
of offenders, who should be isolated or killed. 

ISTests well supplied with straw will minimize the possibility of 
the accidental breaking of eggs, and darkened nests will prevent a 
broken egg from being seen. Craving for lime in the egg shells 
may be forestalled by supplying an abundance of oyster shells and 
bone. 

Feather eating and feather pulling. These habits constitute 
very troublesome vices not only among fowls but also in cage birds. 
A bird may pull out its own feathers or those of its companions. 
The sensation of having the feathers plucked apparently is not dis- 
agreeable, for a bird will stand quietly while another pulls out its 
feathers. Finally the birds taste blood on the emerging feather and 
as a result, never allow a feather to develop. The vice is often 
observed in cage birds such as parrots, among hens that are closely 
confined, and occasionally among hens lacking certain elements in 
the feed. Parasites of the skin are important causes of the itching 
leading to feather pulling. In some instances the eruption of nor- 
mal feathers during molting, occasions an itching sensation and 
starts the habit. Perhaps the most common cause is a monotonous 
diet of a restricted number of elements. Hens at large in warm 
weather can satisfy individual food requirements from among the 



GENEKAL DISEASES 177 

various materials available, siicli as grass, insects and mineral sub- 
stances. 

Klee finds it very useful to supply blood in a cooked form, mixed 
with bran and curd. Under these conditions the birds do not acquire 
a taste for blood. Burned shells and green feed are also desirable 
elements in the ration. Green feed is best surrounded by a wire 
netting in such a way that the birds are compelled to reach through 
the meshes to obtain the feed. In winter time cooked beets or 
sprouted oats may be used. 

Breaking up the habit in parrots often causes difficulty. Daily 
sprinkling with water and providing variety of feed are useful. 
Klee also has observed many cases benefited by smearing the feathers 
with sepia, or unsweetened chocolate and by keeping the bird in the 
dark. It is possible to fit a broad aluminum collar on the neck of 
a parrot in such a way as to prevent the bird from reaching the 
feathers. 

According to Klee, lack of feathers is observed in pigeons from 
time to time without being due to feather pulling. In some in- 
stances the pin feathers are present in the skin but do not break 
through. Persistence of the feather sheath also occurs in pigeons, 
in which case the feathers develop while rolled up in a horny cover- 
ing. Under normal conditions this sheath is shed early in the de- 
velopment of the feather. Sometimes if the bird is kept until the 
molting period the new feathers will develop normally. 

In chickens and in any growing birds, interference with nutrition 
such as intestinal catarrh will cause retardation of the feather de- 
velopment in the molting period. Molting exerts such a drain upon 
the strength of birds that only a well nourished bird is able to molt 
normally. As a result, birds are more inclined to become diseased 
during molting than afterwards. 

REFERENCES 

1. Dickson. Botulism. A cause of liinberneck in chickens. /. Am. 
Vet Med. Ass., Vol. 3, 1917, p. 612. 

2. Hebrant et Antoine. A propos de la goutte ou diathese urique. Ann. 
de Med. Vet., T. 58, 1909, p. 321. 

3. Klee. Die hauptsachlichsten Geflugel-Krankheiten. Leipsig. 1905. 



CHAPTER XVI 

INTERNAL PARASITES 
PAKASITES OF THE ESOPHAGUS, CROP, PKOVEXTEICULUS AND GIZZARD 

FOWLS 

Dispharagus nasutus, a filarial worm 7 to 9 mm. long, is one of 
the most important parasites occurring in the portion of the ali- 
mentary tract of fowls anterior to the gizzard. The worms are 
found in great numbers in the mucosa of the proventriculus and of 
the gizzard. The aftected birds become emaciated and depressed 
without losing appetite. The mucosa of the gizzard has been ob- 
served to be bristling with the parasites, some in the mucosa and 
others attached to the mucosa by one end and floating free in the 
lumen. The proventriculus when infested may be increased to 
double the usual size, becoming spherical in form. The mucosa is 
greatly thickened in places where the parasites are most numerous. 
Cases have been observed in which the worms were so numerous as 




Fig. 10. Spiroptera pectinifera. Male. Caudal extremity. X l"-"^- Neumann) 

to give the glands a villous appearance. Colucci obtained good re- 
sults by the administration of capsules of .5 gram of oil of turpentine 
morning and evening. 

D. liamuloms has been reported from fowls in Brazil as occurring 
in little fleshy excrescences on the surface of the gizzard. D. laticeps 
has been found in the fowl and certain rapacious birds. Physa- 
loptera truncata has been observed in the gizzard of a fowl in Brazil. 

Spiroptera pectinifera is a hair worm which infests the gizzard of 

178 



INTERNAL PARASITES 179 

fowls. Individuals vary from 4 to 9.5 mm. in Icng-th and are 2 
mm. broad. The worms are attached to the mucosa of the gizzard 
by their anterior extremities. The mucosa is covered by a brownish 
deposit 2 to 3 mm. thick, consisting of a mixture of blood and debris 
of the parasites. The affected mucosa shows irregiilar depressions 
which are granulated, reddened and hemorrhagic. The affected birds 
show anemia, progTessive cachexia and good appetite to the last. 
One to three months may elapse between appearance of symptoms 
and death, depending upon the age and vigor of the subject. This 
parasite has been reported as causing heavy mortality among 
chickens in France. Its presence in the gaiinea-fowl has been re- 
ported. 

Eansom has described a nematode worm Gonglyonema ingluvicola 
parasitic in the crop of fowls. The presence of the females may be 
detected by noting the occurrence of small coiled ridges on the sur- 
face of the mucosa, discernible with the naked eye. The males are 
only discovered by the use of a hand lens. Specimens may be ob- 
tained for detailed study by teasing the tissue. The females vary 
from 32 to 45 mm. in length, while the males are from 17 to 19 mm. 
long. The infestation does not so far as known, result in serious 
disturbance of health. The same parasite has been recognized in 
Europe by Oiurea. 

Trichosoma annulatum is a worm 15 to 80 mm. in length which 
has been reported as occurring under the epithelium of the mucosa 
cf the esophagus of the fowl. Another member of this genus, T. no- 
dularis causes serious trouble in waterfowl, 

Displiaragus spiralis, a worm 7 to 9 mm. long has been reported in 
the same location as well as in the gizzard. Prosthogonimus pellu- 
cidus, a trematode, has been found in the esophagus of fowls. 



PHEASANTS 

Trichosoma. sfnimosum, causes serious loss among young pheasants. 

It lives in the large folds of the epithelium of the esophagus and 

sometimes penetrates the mucosa. It 

forms passages in which the female de- _,t|^^^^^^^^^^^^^^^^ 

posits eggs. This destruction of epi- W'T''''^u''^^X^ ^^^^^^ ^^^^ ^i 

thelium occurs in the esophagus, buccal ^""^^ 

• , J J.1 i 1 T"! J • Fio. 20. Trichosoma stnimosuni. 

cavity and the trachea. The disease p,,^^,, interior extremity. 

causes great weakness at the beginning, ( Reibisch ) 
followed by rapid emaciation. Death 



180 DISEASES OF DOMESTICATED BIRDS 

occurs four to six days after the appearance of the first symptoms. 
Treatment consists of administering a 2.5 per cent solution of car- 
bolic acid in the drinking water or in the mash. 

WATERFOWL 

Strongylus nodularis has been reported as occurring in water- 
fowls, most frequently in the mucosa of the gizzard. The female 
worms vary in length from 12 to 22 mm. while the males vary from 
10 to 16 mm. The parasites are about 5 mm. in diameter, and are 
threadlike in form. They are more narrow at the ends, especially 
at the head end. Freese reports a loss of 200 out of 700 geese, due 
to the parasite. 

Symptoms. Single individuals occur very frequently in healthy 
geese without causing symptoms or noteworthy lesions. Extensive 
invasion of young geese is attended with serious results. At the 
beginning of sickness the young geese appear weak, sit most of the 
time and move with reluctance. They make characteristic choking 
movements and soon show more or less diarrhea. The birds have a 
very good appetite and consume their feed ravenously. In spite of 
the large amount of food consumed, the birds gradually become ema- 
ciated almost to skeletons. Finally they fall from weakness and 
are unable to rise again. In this stage the birds stop eating and die 
in a day or so. The whole course of sickness occupies three to eight 
days. The younger the geese, the more they are affected. The 
young, as a rule, die. 

Morbid anatomy. The carcass is excessively emaciated and only 
traces of the breast muscles remain. The mucosa of the small in- 
testine, especially near the gizzard, is reddened, thickened and cov- 
ered with a large amount of viscid mucus. The principal lesions are 
found in the gizzard. Except where the epithelium normally forms 
horny plates, it is covered with a thick, bark-like mass, dark brown 
or dark brownish red in color. The consistency of the mass is more 
or less tough and in some places, is more like mucus. In and under 
this material are innumerable parasites in coils. Kot infrequently 
the worms are attached to the bark-like mass by their heads, with 
the other ends free in the lumen. Sometimes a mucous layer, with 
worms, is located in the lower third of the esophagus. Occasionally 
a few worms may be found on the mucosa of the small intestine. The 
statement of some authors that the parasites occur under the mucosa 
is incorrect, for they occur only under the epithelium and less com- 
monly directly in the epithelium. 



INTERNAL PARASITES 



181 



Displiaragiis uiicinatus has been reported as occurring in the esoph- 
agus and proventriculus of geese, ducks and swans. They occupy 
cyst-like structures which are most frequently encountered in the wall 

of the proventriculus. When these are 
opened the worms are found surrounded by 
a bloody fluid or a yellowish caseous mass. 
The wall of the proventriculus is thickened 
and the mucosa is covered by a large amount 
of yellowish green viscid mucus. A stage of 
the life cycle of the parasite is passed in a 
certain aquatic form, Dapluiia juJex. The 
embryos, free in the stomach of the bird, 
gain access to the water where they are 
taken in by the DapJinia, which creature is 
in turn eaten by the waterfowl. 

Prophylaxis must depend chiefly upon 
killing of infected birds, and upon keeping 
birds away from stagnant water, colored 
brownish or yellowish by the presence of 
Daplima in large numbers. 

Sclerostomum anseris infests the gullet, 
proventriculus and gizzard of geese. It 
burrows under the mucous membrane and 
causes the formation of dark brown crust- 
like layers on the epithelium. In young 
ducks it causes gradual emaciation and debility. The location of 
the parasites discourages the use of antihelminthics. 

Hystricliis tricolor is a worm which infests the proventriculus 
of ducks, and causes extensive destruction of 
tissue. Very large ulcers are formed wdiich al- 
most perforate the walls of the organ. Cysts 
about the size of a bean, containing the parasite, 
are also found. A similar parasite Hystrichis 
elegans also occurs in the proventriculus of 
ducks and of a large number of palmipeds. H. 
ciffini occurs in similar location in the swan. 

Tropisurus fissipinus form cysts in the sub- 
mucous region of the esophagus of ducks, some- 
times causing a fatal inflammation. 

Trichosoma coniortum occurs in ducks and geese besides other 
birds. They infest the dilated portion of the giillet, which in ducks 




Fig. 21. Dispharagus 
uncinatus. Dorsal 
view of anterior ex- 
tremity. Enlarged 60 
times. (Schneider) 




Fig. 22. Hystrichis 
tricolor Cephalic ex- 
tremity, (v. Ratz) 



182 



DISEASES OF DOMESTICATED BIRDS 




and geese, performs the func- 
tions of a crop. The pres- 
ence of the parasites causes a 
distention of the gullet and a 
condition quite similar to dis- 
tention of the crop in fowls. 
The infested birds display ar- 
rested development, emacia- 
tion, difficult locomotion, epi- 
leptic movements, somnolence 
and lack of appetite. Death 
is frequently due to asphyxia 
resulting from over disten- 
tion of the gullet. 

At autopsy it is observed 
that the galleries formed by 
the worms appear as whitish 
curved lines which stand out 
prominent relief against 



m 



the congested mucosa. Mi- 
croscopic examination of the 
tissue will reveal the presence 
in the galleries of the worms 
and their eggs. 

Positive diagnosis is diffi- 
cult during life unless micro- 
scopic examination is made 
of the feces or of water with 
which the crop has been 
rinsed. 



Fig. 23. Trichosoma contortum. A, caudal 
extremity of female; B, eggs from the 
uterus in various stages; C, caudal ex- 
tremity of the male. Enlarged 300 diam- 
eters. (Railliet) 

Treatment may consist of administering two tablespoonfuls of a 
mixture of turpentine with twice its volume of olive oil. 

Filaria cygni has been observed in the intestine and ceca of a 
swan which was exceedingly emaciated. 



TAPEWORMS 



General character. Tapeworms, also designated cestodes, con- 
stitute important parasites of the intestines of birds. When present 
in large numbers they occasion a disease designated tseniasis. The 
individual worm is composed of a head called the scolex and a 



INTERNAL PARASITES 



183 



variable 



segments 



designated 




Fig. 24. Segment of Davainea echino- 
bothrida showing the reproductive or- 
gans. Enlarged. (Ransom) 



number of 

proglottides. The 
scolex is armed with a series of 
hooks by which it becomes at- 
tached to the intestinal mucosa 
of the host. Each proglottid or 
segment of the worm is virtually 
an individual and is bisexual. 
The segments are not provided 
with an alimentary canal, but 

absorb nourishment directly from the intestinal contents of the host. 
As the terminal segments in turn mature, they are separated from 
the worm and are discharged in the droppings. 

Species of cestodes. A large number of species of tapeworms 
have been reported as occurring in the intestines of domesticated 
and wild birds. Kansom has examined nine species in American 
chickens and turkeys as follows : In chickens, Hymenolepis carioca, 
Choanotaenia infundihulum, Davainea tetragona, D. echinoboihrida, 
D. proglottina, Amoehotaenia sphenoides; in chickens and turkeys, 
D. cesticillus, Hymenolepis cantaniana; in turkeys, Metroliasthes 
lucida. He notes that the tapeworms of American ducks, geese, and 
pigeons have not yet been investigated. Neumann lists four more 
species as having been found in fowls. These are Cotugnia diagono- 
pora. Taenia fasciolaris, T. exilis and Bothriotaenia longicollis. 

Tapeworms found in the various birds are listed by Neumann as 
follows : 

Turkey: Choanotaenia infundihulum, Metroliasthes lucida, 
Davainea cantaniana, D. cesticillus, D. friedbergeri, Hymenolepis 
carioca, H. musculosa, H. meleagris. Not named. 

Pheasant: Choanotaenia infundihulum, Davainea echinohoth- 
rida, D. cantaniana, D. friedhergeri, Hymenolepis phasianina. 

Pigeon : Choanotaenia infundihulum, Davainea echinohothrida, 
D. crasmla, Bertiella delafondi. 

Duck : Hymenolepis anatina, H. gracilis, H. sinuosa, H. coronula, 
H. parvula, H. megalops, H. lanceolata, Choanotaenia infmidibulum, 
Davainea crassula, Flmhriaria fasciolaris. 

Goose : Hymenolepis lanceolata, H. setigera, H. gracilis, H. 
fasciata, H. sinuosa, H. teriuirostris, Fimhriaria fasciolaris. 

Neumann considers tapeworms as occurring infrequently in pig- 
eons and rarely present in sufficient number to cause trouble. In 
ducks they exert feeble pathogenic action. Hymenolepis setigera and 



184 DISEASES OF DOMESTICATED BIEDS 

H. lanceolata, singly or together cause injury among geese in Europe. 
Davainea friedhergeri causes great losses among pheasants. 

Life history. From time to time the tapeworm in the intestine 
of the chicken discharges ripe segments filled with eggs, which are 
voided in the feces. To maintain the life cycle it is necessary tliat 
the tapeworm eggs be taken with the food into some creature known 
as a secondary host. In this host the embryos escape from the eggs 
and migrate to some organ where they form a cyst-like structure 
known as a cysticercoid. The life cycle is completed in case the 
intermediate host is eaten by a chicken in which event the cysticercoid 
develops into the adult form. 

Comparatively little is known about the secondary hosts of tape- 
worms of poultry. Of the five species of tapeworms that have been 
reported in chickens in the United States, tlie intermediate host of 
but one has been discovered. It has been determined that the inter- 
mediate host of Choanotcenia infundihulum is the common house 
fly, Musca domestica. 

The intermediate hosts of a number of tapeworms of birds re- 
ported as occurring in other countries have been discovered. Thus 
a slug is necessary for the life cycle of Davainea 'proglottina,. a 
chicken tapeworm. The intermediate hosts of certain tapeworms 
of the duck have been found to be various species of fresh water 
crustaceans. 

In general, the intermediate host is to be sought among the various 
insects and other forms of animal life to which the infested birds have 
access such as snails, insects, crustaceans or worms. 

Symptoms. These vary to some extent in different birds ac- 
cording to age and the degree of infestation. A few worms are not 
harmful to the bird and can hardly be noticed. Young birds are af- 
fected more seriously than old ones. In moderate infestation the 
bird is always hungry and experiences excessive thirst. Restless- 
ness is marked and doubtless accounts fur the lean condition of the 
bird. Heavily infested birds show such symptoms as drooping 
wings, emaciation, rutHed feathers and isolate themselves from the 
flock. 

The condition of the feces is more or loss altered in tapeworm in- 
festation. Heavy infestation causes inliammation of the intestine 
and diarrhea with mucous droppings. The secretion is at first clear, 
transparent, semi-liquid and slighily \>..,;su in coLr, Later the 
mucus becomes brownish yellow in col r xiio to hemorrhage caused 
"loy the worms, and this coloration cons itiues one of the most char- 



INTERNAL PARASITES 



185 



acteristic symptoms. When the bird is very heavily infested, gas 
bubbles are observed in the droppings, and remain visible for some 
time. 

Segments of tapeworms may be found in the feces by careful 
search, and microscopic examination may be utilized for detecting 
the presence of tapeworm eggs. 

Tapeworm infestation in geese has been reported in Germany as 
causing very marked nervous symptoms. The birds walk very lit- 
tle and assume an upright position like that of the penguin. 

Morbid anatomy. In excessive infestation the carcass is anemic 
and emaciated. On slitting the intestine, worms will be found in 

greater or less number 
throughout its whole ex- 
tent between the gizzard 
and the ceca. They are 
attached to the mucosa by 
their heads and may cause 
more or less inflanunation. 
The most serious patho- 
logical changes are caused 
b}'' infestation with Davav- 




Fic. 25. Gravid segment of Davainea echino- 
bothrida. Enlarged. (Ransom) 



7iea echinohothrida which results in the 
formation of nodules in the intestine. 
This condition has been described by 
Moore under the name of nodular tsenia- 
sis. The nodules are most numerous in 
the lower third of the small intestine. 
Exceptionally they occur in the duode- 
num and colon. In severe infestation 
the presence of nodules causes numerous 
protuberances from the serosa, varying 
in size from those barely perceptible, to 
elevations 4 mm. high. The color varies 
from pale or dark yellowish in the larger 
ones, to the normal gray of the serosa 
shown by the smallest ones. Similar elevations are observed on the 
mucosa of the intestine. Small tapeworms occur attached to the 
mucosa over the nodules. Over some of the nodules there are areas 
in which the mucosa has sloughed, leaving ulcers. 

The contents of the larger nodules consist of greenish yellow, ne- 
crotic material which on section has a glistening, homogeneous ap- 




FiG. 26. Head of Davainea 
echinohothrida. Enlarged. 
(Ransom) 



186 DISEASES OF DOMESTICATED BIRDS 

pearance. Surrounding this, there is a thin layer of infiltrated tis- 
sue. The smaller nodules contain a substance more resembling pus, 
and in these the microscopic study of sections most readily reveals the 
presence of tapeworm heads. The penetration of the intestinal wall 
by the heads induces infiltration and eventually results in the forma- 
tion of nodules. 

Diagnosis. The chief points to be relied upon in diagnosis are 
emaciation, excessive appetite and thirst together with the character- 
istic yellowish-brown color of the droppings. The detection of tape- 
worm segments in the feces is best done by immersing the suspected 
white mass in water. If it consists of urates alone, it will be dissi- 
pated in fine granules, while the worm segments will be recognized as 
firm masses. Some of the general symptoms of unthriftiness are 
also indicative of nematode infestation, but in this case the birds 
often pass blood. Ultimate decision will rest upon the information 




Fig. 27. Hymenolcpis lanceolata. Natural size, in a medium state of extension. 

(Railliet) 

yielded by an autopsy. The intestine should be opened while im- 
mersed in warm water, to facilitate recognition of the worms. They 
will be found attached to the mucosa, and vary in size from micro- 
scopic objects to worms four or five inches long. 

Treatment. Turpentine is held in high repute as a tseniafuge 
and has the additional advantage of expelling round worms also. 

The fowls are fasted for twenty-four hours during which time 
they should receive a dose of Epsom salts. One teaspoonful of salts 
is allowed for each bird, the whole being dissolved in warm water and 
mixed with mash. Greater accuracy of dosage will be assured if the 
dose is administered directly to each bird. The most convenient sys- 
tem of carrying out the vermifuge treatment is to withhold food in 
the morning and give the salts in the evening. The following morn- 
ing the turpentine should be given in a dose of from one to two 
teaspoonfuls per fowl. Owing to the offensive qvialities of turpen- 
tine it is not possible to give it in food, but it must be administered 
to each bird individually. The most expeditious method is to inject 
the dose directly into the crop with a hypodermic syringe. A slower 



INTERNAL PARASITES 



187 



method is to introduce the dose into the crop by means of an oiled 
rubber tube inserted through the oral cavity and esophagus. The 
turpentine, diluted with an equal amount of olive oil may be ad- 
ministered by the mouth. If the mixture is given slowly with a 
spoon or medicine dropper the bird will swallow it naturally and will 
cause very little trouble. Three or four hours after giving the tur- 
pentine, the birds should receive another laxative dose of salts ad- 
ministered in a mash as before. 

Owing to the habit of burying their heads in the intestinal wall, 
tapeworms are very resistant to treatment. Consequently it is ad- 
visable to repeat the vermifuge treatment in about three weeks. 

Gutberlet reports favorably upon the use of lye for expelling tape- 
worms. A tablespoonful of concentrated lye was added to one gal- 
lon of a mixture of wheat and oats 
which was cooked slowly for two 
hours. Fifteen birds, after fasting 
for about fifteen hours, were allowed 
to eat the mixture. A second dose 
is given twelve hours after the first 
one. 



A number of other substances are 
employed to e^^pel tapeworms, but 
some fail on account of having lost 
their active properties. Areca nut 
in doses of 30 to 45 grains may be 
administered to fowls in the form of a pill, but turkeys do not tol- 
erate this remedy well. 

Powdered pomegranate root bark may be fed to fowls in a dose of 
one teaspoonful to each 50 birds. It may be followed by a purgative 
dose of 2 or 3 teaspoonfuls of castor oil per bird. Male fern in a 
dose varying from 30 grains to 1 dram of the powder may be given 
morning and evening before feeding. 

Megnin recommends treating pheasants for tapeworm with kamala, 
mixed into a paste with hard boiled eggs and bread. 

Prophylaxis. An accurate knowledge of the secondary host for 
each species of tapeworm, might suggest very effective preventive 
measures but in the absence of much of this information, such 
measures must be of a general nature. It is desirable to collect 
the droppings and treat with lime. Lime or ashes may be scattered 
over the droppings under the roosts. General sanitary measures 




Fig. 28. Hymenolepis lanceolata. 
A, cephalic extremity, enlarged 
100 times; B, egg enlarged 300 
times. (Railliet) 



are of value, and particularly, the practice of moving birds to new 



188 DISEASES OF DOMESTICATED BIKDS 

ground should be encouraged. The knowledge that the house fly is 
the intermediate host of a chicken tapeworm suggests the advisability 
of combating that insect. It breeds commonly in bird or horse ma- 
nure and any decaying vegetable matter. These breeding places 
should be eliminated as far as possible besides using fly traps. 



ROUND WORMS 

General nature. Eound worms or nematodes are common para- 
sites of the intestines and are capable of inflicting considerable 
damage. They are long, slender and thread-like in form. Mouth, 
alimentary canal and anus are present. The female worm is gener- 
ally larger than the male. 

Species of round worms. There are two principal species in 
fowls. Ascaridia (HeteraMs) perspicillum occurs in the small in- 
testine. The male is 3 to 8 cm. long, while the female is 6 to 12 cm. 
in length. The color of the body is yellowish white. They are often 
present in numbers sufficient to occlude the lumen of the intestine. 
The same species is found in the turkey and guinea-fowl. Heter- 
aMs papillosa, a much smaller worm with white body, is very com.- 
mon in the ceca. The male is from 7 to 13 mm. long while the fe- 
male varies from 10 to 15 mm. in length. This species is found 
also in the turkey, guinea-fowl, peafowl, and pheasant. Five other 
less important species, Heterakis lineata, H. brasiliensis, H. compar, 
H. cojyipressa and //. differens have been reported by J^eumann as 
occurring in fowls. This writer lists other nematodes of the intes- 
tine as follows : 

Pigeon : Heterakis columboe. 

Duck: Ascaris crassa, Heterakis dispar, H. vesicularis, H. 
lineata,. Strongylus tenuis. 

Goose: Heterakis dispar, H. vesicularis, Strongylus tenuis, Tri- 
chosoma anatis. 

Life history of Ascaridia perspicillum. Eggs are deposited by 
the worms within the intestine and are expelled in the feces. The 
length of time worm eggs will remain alive in the droppings is not 
fully determined, but there is evidence that they are viable up to a 
year. The life cycle of the worm is completed by eggs gaining access 
to a fowl through contaminated feed or water. Ordinarily, eggs do 
not hatch until they are taken into the alimentary canal of a fowl. 
The worms require three to four weeks to develop into sexually ma- 
ture forms. 



INTERNAL PARASITES 189 

Symptoms of Ascaridia infestation. Affected birds appear un- 
thrifty and emaciated. Either diarrhea or constipation may occur. 
The affection is most severe in young birds. 

Treatment. Beach conducted experiments with a number of 
remedies to determine their vahie in causing the expulsion of the 
worms and came to the conclusion that tobacco stems are most ef- 
ficient. For one hundred fowls he takes one pound of finely chopped 
tobacco stems and steeps them for two hours in enough water to keep 
the mass covered. The liquid and the stems are mixed with half 
the amount of ground feed usually allowed the birds for one feed- 
ing. On the evening before the day of administering the remedy, 
the birds should be fed only half a ration and they should be kept 
without feed until afternoon of the following day. Then the mixture 
of tobacco and feed is given and under the circumstances is sometimes 
readily eaten. Occasionally, fowls refuse the mixture. Two hours 
later, the birds are given a quarter size ration of ground feed mixed 
with water containing eleven ounces of Epsom salts for each hundred 
birds. ISFo difference of dosage to correspond to birds of different 
ages is attempted, for the matter is adjusted by the amounts of the 
mixtures that the birds can eat. Reasonable care should be exercised 
to make certain that birds have equal opportunity to eat. The treat- 
ment is calculated to cost about ten cents per hundred fowls. 

The same procedure should be repeated in two weeks which has 
been found to be sufficient to free the birds entirely from parasites. 
Difficulty in administering the treatment is sometimes encountered 
because the birds will refuse to eat the mash containing the tobacco. 

Theobald recommends thymol as an agent against nematodes. The 
dose for the fowl is .06 gram given in the form of a pill. Two or 
three hours after giving the thymol, a teaspoonful of olive oil is 
administered. 

Megiiin recommends administering santonin in the food in a dose 
of 4 to 5 grams for every ten birds. 

Klee recommends 5 to 10 drops of anise oil in 1 to 2 teaspoonfuls 
of olive oil, also 4 to 6 drops of benzol with oil. 

Prophylaxis. Thorough disinfection of the yards and quarters 
is necessary in order to minimize the possibility of reinfection from 
worm eggs that have been deposited in the feces. Ilerms and Beach 
have determined that worm eggs are found only in the top two inches 
of the soil of infected yards. After sweeping the yard and removing 
rubbish the area was treated with a 1 : 1000 solution of bichloride 
of mercury. About one gallon of solution to each ten square feet of 



190 DISEASES OF DOMESTICATED BIRDS 

soil was found necessary to secure penetration of the fluid to a depth 
of two inches. A trial of the effectiveness of the treatment in pre- 
venting the reinfection of birds that had been freed of worms yielded 
evidence of its value. Such birds increased in size rapidly and post 
mortem examination of the poorest specimens after three weeks 
yielded no evidence of worms. Other fowls on a control area, not 
disinfected, became seriously infested in a similar length of time. 

Bichloride treatment of roosting houses and other buildings to 
which birds have access, is indicated. Netting under the roosts is of 
value in keeping birds from contact with feces. 

Round worms in the pigeon. HeteraJcis coluniboe occurs in the 
intestines of pigeons in enormous numbers. As many as 400 to 500 
worms have been observed in one individual. The infestation causes 
loss of appetite, periodic mucous diarrhea and emaciation which is 
particularly marked in the pectoral muscles. At 
autopsy the worms are observed packed closely to- 
gether. The mucosa is distended in patches which 
are engorged with blood and ulcerated. These 
areas are covered with thick mucus. Occasionally 
the parasites perforate the wall of the intestine and 
are found in various parts of the thoracic and ab- 
dominal cavities. Treatment advised by Ziirn con- 
sists of administering 6 centigrams of calomel in 

Fig. 29 Hetera- ^j^g form of pills with bread or with butter. More 
kis columbce. A, . ^ i • i 

male; B, female, serious cases may be treated with areca nut m 1 

"'^^y.^^l. s i ^ ® • gTam doses, given in the same manner. Two hours 

after administering the pills, each bird is given a 

teaspoonful of castor oil. The affected birds may be given a weak 

decoction of garlic to which one-half per cent of sodium salicylate 

has been added. 

Strongylus quadriradiatus has been observed by Stevenson in the 
intestine of the pigeon. The presence of a few worms causes no 
harm, but large numbers cause harm attributed to injury of the wall 
of the intestine permitting subsequent invasion by bacteria. 

TKICHOSOME INFESTATION OF CHICKENS 

Several worms of the genus Trichosoma have been described as 
harmless inhabitants of the intestines of fowls. However, Freese 
has observed that Trichosoma retusum, is capable of causing great de- 
struction among chickens. The same parasite has been reported in 
the guinea-fowl. The worms vary from 13 to 19 mm. in length 




INTERNAL PARASITES 191 

and from .06 to .07 mm. in breadth. Other species reported in the 
fowl are T. collar e, T. duhium, T. caudinflatum and T. gallinum. 

Symptoms. The chickens become less lively, allow the wings to 
droop and show diarrhea. The appetite is at first very good but later 
becomes poorer. There is increased thirst. The bird becomes more 
and more emaciated and finally can hardly move because of loss of 
strength. Without treatment the disease usually ends fatally. The 
duration of the disease varies from three to ten days according to the 
resistance of the victim. 

When old hens are affected, they show similar symptoms. At the 
beginning of sickness egg laying drops off and soon stops entirely. 
The disease in hens runs a course of 2 to 4 weeks. 

Morbid anatomy. The carcass is greatly emaciated and 
anemic. All organs with the exception of the intestinal canal, are 
free from lesions. The mucosa of the small intestine throughout 
its whole extent is covered with a grayish yellow exudate. The mu- 
cosa is thickened and reddened on the surface by short streaks and 
points. The contents of the ceca and rectum are thin and viscid. 
Innumerable trichosome worms are present on the mucosa of the 
small intestine throughout its whole extent, and a few also occur in 
the ceca. 

Diagnosis. The disease caused by the trichosomes can be recog- 
nized with certainty only by autopsy. On account of the hair-like 
fineness of the worms they can only be discovered after the closest 
scrutiny. The contents of the intestine are teased with a needle, or 
the needle is stroked over the mucosa. If the worms are present, it is 
likely that several will adhere to the needle. Another method is to 
remove a portion of the exudate from the mucosa and mix with 
water. The hair-like worms may be detected with the naked eye. 
In any event it is desirable that microscopic examination be made. 

Treatment. Freese recommends the administration of oil of 
anise in early stages of infestation. On each of two successive days 
each chicken is given a dose of 5 drops of etherial oil of anise in 1 
teaspoonful of olive oil. Old hens require twice as much anise oil. 

Trichosomes in the pigeon. Trichosoma columbce is fre- 
quently found in the large intestine of the pigeon. It is capable of 
causing an intense intestinal catarrh. It may be present in colossal 
numbers in the intestine causing the mucosa to show tumefaction, in- 
filtration, petechiae and red streaks. 



192 DISEASES OF DOMESTICATED BIRDS 

FLUKES 

General nature. Trematodes (flukes) are hermaphroditic worms 
possessing suckers by which they become attached to the mucosa of 
the intestine of the host. The intestinal tract ends blindly without 
an anus. In the temperate zone they are generally harmless and 
uncommon parasites. 

Species and hosts. ISTeumann states that Echinostomum echin- 
atum occurs in the fowl, duck, goose and swan ; E. conoideum in the 
fowl, duck and goose; E. recurvatum in the fowl and duck; Clino- 
stomum commutatum in the fowl, turkey and pigeon ; N otocotyle ver- 
lucosa in the fowl, duck and goose. Bunodera linearis has been re- 
ported in the fowl alone, Cyclocoelum mutabile in the turkey alone, 
while Holostomum gracile and H. splicer ocephalum occur in the 
duck alone. 

THOKN HEADED WORMS 

Three species of the genus Ecliinorhynchus occur in ducks but only 
one has been reported as causing injury. 

Echinorhynchus polymorphus is fusiform in shape and colored or- 
ange red. The anterior extremity of the worm is provided with an 
ovoid proboscis armed with eight rows of hooks. The male worm 
measures 4 to 6 mm. in length while the female varies from 15 to 25 
mm. in length. The wonns usually are fixed firmly to the wall of the 
intestine. 

Before opening the intestine the serous surface of the same is 
seen to be covered with numerous nodules, the centers of which are 
orange colored. On opening the intestine the mucosa is found 
studded with worms of the sam-e color attached by their anterior ex- 
tremities. Their presence sets up a severe inflammation of the mu- 
cosa and causes the formation of the nodules on the serous surface. 
The condition described often causes diarrhea, emaciation and 
anemia. 

The same species occurs in the swan. E. filicollis and E. spwro- 
cephalus are found in the duck. 

FLAGELLATES 

Flagellated protozoan organisms constitute a small number of 
forms parasitic in the intestines of birds. These are nucleated 
bodies provided with one or more flagolla and sometimes possess an 
undulating membrane. Neumann lists the following species : Tri- 
chomonas eherthi has been observed in the glands of Liebcrkuhn of 
a duck and in a goose. It is little known and without pathogenic 



INTERNAL PARASITES 193 

importance. T. columhce lias been reported as causing the forma- 
tion of caseous foci in the liver of the pigeon with fatal result. 
Moiias (Monocercomomis) anatis has been reported as occurring in 
the small intestine of the duck. Martin and Ivobertson have studied 
the flagellates of the ceca of fowls dividing them into the four 
species: Chilomastix gallinarum, Tricliomorias gallinarum, T. 
eherthi and I'richomastix gallinarum. 

Hadley observes that the intestinal fauna of any young turkey 
after it has been on the gTound for a few days will contain a variety 
of protozoan parasites. Among these, the most common are flagel- 
lates, certain sporozoa and amebas. At least three types of flagellates 
are usually present, Trichomonas, Chilomastix and Lamhlia. He 
considers that Trichomonas plays a pathogenic role in cecal and he- 
patic infection in birds comparable to intestinal and hepatic ame- 
biasis as observed in mammals. Hadley considers the flagellates de- 
scribed by him as identical with bodies described by Theobald Smith 
under the name Amoeba meleagridis and the cause of blackhead in 
turkeys. He regards Trichomonas as a facultative parasite in that 
under certain conditions it exists as a harmless, ever-present intes- 
tinal parasite. According to this view the Trichomonas under cer- 
tain unknown circumstances invades the tissues and causes disease. 

Trichomoniasis of chicks. Weinzirl has described a highly fa- 
tal disease of chicks attributed to a new species designated Tricho- 
monas pullorum. 

Symptoms. Chicks under a month old only are attacked. The 
disease most commonly appears about the tenth day after hatching. 
The affected birds droop, they huddle together, the wings drag, the 
eyes are closed and the skin of the head is pale. Acute cases suc- 
cumb in a day or two without showing diarrhea. Other cases be- 
come chronic, in which stage diarrhea is present. The temperature 
is subnormal and is usually about 102° F. The disease is not ob- 
served until late spring and summer. 

Morbid anatomy. Autopsy reveals no lesions except a gen- 
eral anemic condition. The ceca may be slightly enlarged and the 
contents thin and slimy. The parasites collect in the crypts of the 
mucosa frequently in pure culture. When diarrhea exists, the pro- 
tozoan may be found in the intestine and in the voided mucus. 

Etiology. The flagellate Trichomonas pullorum regarded by 
Weinzirl as the cause of the chick disease occurs in two forms. One, 
the pear shaped type moves about actively by means of flagella and 
also exhibits active ameboid movements. This type varies from 3.5 



194 DISEASES OF DOMESTICATED BIRDS 

by 7 microns to 5.5 by 9 microns, and is the only form occurring in 
the cecal crypts. The globular form occurs in the lumen of the ceca. 
Control of disease. Feeding of sour milk is favorably regarded 
as a means of saving life. 

PAKASITES OF THE LIVER 

The liver of birds is rarely subject to parasitism, if entero-hepatitis 
of the turkey be excepted. 

A flagellate Cercomonas hepatica has been reported in the liver 
of squabs, causing yellowish nodules. 

Echinococcus polymorplius, the cystic phase of the tapeworm of 
the dog, occurs sometimes in birds, and exhibits a preference for the 
liver. Echinococci have been reported in the goura, the peafowl and 
the turkey. The liver becomes enlarged by the presence of the 
cysts until it occupies a large part of the abdominal cavity. The 
hepatic tissue is reduced to thin pieces between the cysts. 

Three species of flukes, Opisthorchis simulans, Metorchis xantho- 
somiis and Billiarziella polonica have been found in the hepatic 
canals or biliary vesicles of the domestic duck. The latter species 
occurs in the blood of a large number of species of wild ducks. 

Heterahis columhcc, normally a parasite of the intestines of pigeons, 
has been reported as occurring in nodules in the liver. 

Blastomycosis. Martin and Daille have described lesions in the 
liver of the goose, due to Blastomyces (Cryptococcus) anseris. The 
parasites are contained in small sacs about the size of a pea, attached 
to Glisson's capsule. These sacs are yellowish white in color, fluctu- 
ate on pressure and are connected with one another by narrow chan- 
nels. The contents of the sacs consist of a yellowish white gelatinous 
material enclosing the blastomyces. These latter consist of round or 
oval nucleated refractile bodies surrounded by a distinct membrane. 

PARASITES OF THE BURSA OF FABRICUS 

According to ISTeumann, the bursa of Fabricus harbors species of 
flukes of the genus Prostliogonimus. They are encountered there but 
rarely, for that pouch disappears in the adult. The parasites conse- 
quently are obliged to leave that diverticulum and enter some of the 
other canals connecting with the cloaca. Sometimes they enter the 
rectum, or they may penetrate the oviduct and become enclosed in an 
eg^g. Probably all the forms found in the oviduct and the egg also 
occur in the bursa of Fabricus. 



INTERNAL PARASITES 195 

Prostliogonimus ovatus occurs in the bursa of Fabricus of a large 
number of birds. It has been found in the oviduct of the hen and 
many observers have found it in hen's eggs. Pr. pellucidus and Pr. 
japonicus have been found in eggs. Pr. cuneatus has been reported 
as occurring in the oviduct of a pea hen. 

COCCIDIA 

Coccidia occurring in the intestines are discussed under the head- 
ing coccidiosis, page 127. 

PARASITES OF THE NASAL CAVITY 

A species of mite of the genus Ehinonyssus infests the nasal cavity 
of fowls, causing a sort of coryza. The mites also occur in squabs 
which sometimes succumb to the parasite. 

Stemostomum rhinolethrum occurs in the nasal fossae of the duck. 

A leech Hemiclepsis tessellata occurs in the nasal and oral cavi- 
ties of geese and ducks, attached to the mucosa. The parasites also 
attach themselves in the eyes, esophagus, larynx and trachea. The 
affected birds are tormented by the presence of the parasites and 
rapidly become emaciated. Megnin recommends applying a two per 
cent salt solution to cause the detachment and death of the parasites. 

A fluke Cyclocoelum arcuatum is reported as a harmless parasite 
of the infraorbital sinus of the domestic goose. 

GAPE WORMS 

Gapes is caused by the roundworm designated Syngamus trachealis 
which attaches to the mucous membrane of the trachea and causes 
jsevere inflammatory changes. These lesions and the additional 
factor of mechanical blocking of the air passages may cause death. 
The air sacs are sometimes infested. 

Species affected. The fowl, pheasant, turkey, peafowl, pigeon, 
certain cage birds and a considerable number of wild birds have been 
reported as hosts of Syngamus trachealis. The adult turkey appears 
to be very much more frequently infested than the adult fowl. Ran- 
som found about 23 per cent of a number of turkeys infested when 
no parasites were found in 635 chickens examined. A related species 
8. bronchialis occurs in the trachea, air sacs and bronchi of young 
geese. 



196 DISEASES OF DOMESTICATED BIRDS 

General character. The female worais are about four-fifths of 
an inch in length and reddish in color. In most cases, the male, 
about a quarter of an inch long, is in copulation, attached to the 
female near the anterior extremity. Thus the appearance of a 
forked worm is induced. 

Symptoms. The presence of the worms is indicated by the 
peculiar wheezing cough, gasping and the expulsion of frothy saliva 
from the beak. The birds appear dull with ruffled feathers, lose 
appetite, breathe with difficulty and display cachexia. Spontaneous 
recovery is rare, and in the absence of treatment the parasites cause 
heavy mortality. Only young birds experience harm from their 
presence. 

Morbid anatomy. The presence of the parasites in the air 
passages enveloped in foamy mucus is the most important feature 
observed at autopsy. The point at which the parasites adhere ofteti 
consists of an abscess filled with yellow colored pus of caseous con- 
sistency. Such an abscess may cause asphyxia. 

Life history. The sexually ripe females are expelled by cough- 
ing, whereupon the eggs are disseminated by the disintegration of 
the female. Thus water and soil become contaminated with the 
larvae hatching from the eggs. It is not believed that an intermediate 
host is necessary in the life cycle of the parasite, even though it has 
been shown that the feeding of earthworms will induce the disease 
among chicks otherwise protected against infection. Undoubtedly 
earthworms may contain larvse in the intestinal tract, due to earth 
ingested by them, without however, playing the role of a host. It has 
been demonstrated repeatedly that chicks may be infected by drink- 
ing boiled water artificially infected with ova and young gape worms. 
The j^oung worms may live for some time in water, and the per- 
sistence cf the infection is favored by a wet soil. Infection undoubt- 
edly occurs through ingestion. The embryos probably make their 
way frcm the gullet or crop, to the trachea by perforating the walls 
of the organs in question. 

Treatment. The practice of dislodging the worms by the appli- 
cation of various remedies applied by inserting the tip of a feather 
into the trachea and twisting, is. widespread. The small size of the 
trachea in young chicks and the fact that some worms are located at 
i^s lower extremity out of reach, makes the operation painful and 
uncertain in its results. Among the remedies applied are oil of 
cloves, oil of turpentine thinned with double its volume of olive oil 
;'nd kerosene oil. The feather also acts mechanically in dislodging 



INTERNAL PARASITES 



197 



the parasites, whereupon they are expelled by coughing. A coiled 
horse hair is frequently employed for the same purpose, but like the 
feather its use is dangerous to the chick. A few worms may be 
caught with tweezers if the larpix is raised high enough. 

It has been asserted that pounded garlic in the proportion of one 
bulb per day added to the food of ten birds would result in the ex- 
pulsion of the worms. Asafoetida has been administered in the food 
with the idea that the agent, eliminated through the air passages, 
would kill the parasites. 

Fumigation with various agents has been employed. Exposure to 
sulphur fumes has been used to induce coughing and expulsion of 
the worms but is dangerous. Affected birds may be exposed to 
tobacco smoke until they become almost insensible, after which they 
are allowed to recover in the open air. Fumes of heated carbolic 
acid have been employed. 

Klee has great confidence in intra-tracheal injection which re- 
quires no more time than other more dangerous kinds of individual 
treatment and is regarded as more effective. The affected bird is in- 
jected in the trachea with 1 c.c. of a 5 per cent aqueous solution of 
sodium salicylate, administered with a hypodermic syringe. This 
fluid simultaneously loosens all the parasites occurring there and a 




Fig. 30. 



Apparatus for making injections in trachea, a. Syringe; b, Straight 
canula; c. Curved canula. (Klee) 



198 DISEASES OF DOMESTICATED BIRDS 

violent cough will expel them. The operation in question can be 
performed by one person, for a syringe with two rings on the barrel 
can be guided easily with one hand. The sick bird is held between 
the knees with the breast in front. The neck is bent up and back 
with the left hand and the trachea lies between the thumb and index 
finger. N^ext, the syringe lying conveniently, is grasped with the 
right hand. The needle is placed near the trachea, after which with 
necessary care it is inserted into the trachea slanting downwards and 
the injection made quickly. The introduction of a dull canula into 
the glottis through the beak is even more suitable than the foregoing 
method. After the injection the bird suffers a light attack of 
choking but soon recovers. 

A very safe but a somewhat less effective remedy is to cause the 
affected birds to breathe air containing finely powdered chalk and 
camphor. Theobald recommends a mixture of two parts by weight 
of powdered chalk and one part of powdered camphor. This is 
dusted into a closed box in which the chickens are confined. 

Prevention. Contaminated water and soil are to be regarded as 
the chief sources of infection. Infectious larvae have been kept alive 
for a year in moist soil. Chicks raised on board floors and thus iso- 
lated from the soil with separation from older birds until a month 
or six weeks old, will escape infection provided the water and food 
supply are not infected. Rotation in the use of land to which chicks 
are allowed access is a valuable practice in avoiding the use of con- 
taminated soil from year to year. Above all, chickens should not be 
kept on soil that has been occupied by turkeys within a year or so. 
Disinfection of drinking vessels and of soil, so far as possible, de- 
serves consideration. Salicylate of soda, 3 drams to the quart of 
drinking water is said to kill the embryo worms. Contaminated soil 
may be disinfected by drenching with a one per cent solution of sul- 
phuric acid. Wet areas should so far as possible be dried by drain- 
ing. 

The isolation of the sick and thorough disposal of the dead are 
obvious precautions. 

THE AIR SAC MITE 

Cytoleichus (Cytodites) nudus has a wide distribution in the 
United States and Europe affecting a large number of gallinaceous 
fowls and also pigeons. The mites are barely large enough to be de- 
tected by the unaided eye. They have been observed in the trachea, 



INTERNAL PARASITES 



199 



lungs, air sacs, hollow bones and the peritoneum. They have been 
reported as occurring exceptionally in the heart, liver and kidneys. 

Their presence within tissues is 
not readily explainable since 
their structure is not adapted to 
the penetration, of tissue. They 
are most commonly noted in the 
air sacs. Hens apparently in 
perfect health may be heavily in- 
fested, so that the economic im- 
portance of the parasite seems to 
be not very great. The method 
of transmission has not been thor- 
oughly explained. Their exit 
from the body could occur 
through the trachea by expulsion 
during coughing. 

Fig. 31. Cytodites nudus. Male, ven- A few writers have obsei-ved 
tral aspect. Enlarged 100 times, cases in which the parasites ap- 
pear to be of pathological impor- 
tance. Gerlach regarded them as the cause of enteritis as did also 
Zundel. Williams attributed high importance to them as a parasite 





Fig. 32. Cytodites nudus. Ovigerous female, ventral aspect. Enlarged 100 

times. (Railliet) 



200 DISEASES OF DOMESTICATED BIKDS 

of fowls in Montana, a view that Wilcox was not able to confinn. 
Among the later observers Walker has reported npon two autopsies 
of fowls in Grahamstown, Cape Province, in which lesions occurring 
in the lungs, were in his opinion, the cause of death. The owner 
reported that the comb turned purple, appetite was lost and the birds* 
seemed fretful and weak in the legs. Birds were noticed to be sick 
for a week, when sudden collapse occurred. Observations bv Walker 
follow. 

Morbid anatomy. Cytodites are frequently found in the thorax 
and peritoneal cavity, fairly frequently on the mesentery and in the 
trachea. The lungs are mottled in appearance by some purple 
patches .2 to .3 cm. in diameter. On section, hyperemia is observed 
and serous fluid exudes from the cut surfaces. Small miliary 
tubercles of a gelatinous consistency are scattered through the af- 
fected portion of the lung, and parasites are visible in the midst of 
each of these. The larger bronchi and some of the bronchioles con- 
tain an exudate in which the parasites are imbedded. Other organs 
and blood appear normal. The conditions observed warrant the 
pathological anatomical diagnosis of hyperemia and edema of the 
lungs, and bronchial pneumonia. 

Microscopic examination of sections of stained tissue, under 300 
magiiification shows that the lung tissue surrounding the invaded 
air passages is infiltrated with leucocytes and red blood corpuscles. 
The blood vessels are congested. Some of the 
parasites have wandered from the air conduits 
into the surrounding parenchyma breaking 
down the regular network conformation of the 
latter. In some of the invaded air passages, 
the parasites have lodged themselves in the 
inner lining and have broken it down. In 
places cytodites are to be seen in the inter- 
lobular fibrous tissue. The larger bronchi 

contain an exudate. 
Pig. 33. DitJii/ridhim 
variabile. fi'om a fowl. 

Enlarged 10 to 12 CESTODE CYSTS IN TIIE LUNGS 

times. (Neumann) 

^N^eumann has described a case in which the 

encysted parasite known as D ithyridium variabile occurred in great 

numbers in the lung of a fowl. These represent the cystic stage of 

a tapeworm, which has not been identified with the adult form. The 

cysts were observed in the inferior surface of the lungs in the an- 




INTERNAL PARASITES 201 

terior and posterior diaphragmatic reservoirs. They were globular 
or ovoid bodies 3 to 4 mm. in diameter, somewhat transparent and 
filled with a colorless liquid containing a parasite. Some were free, 
and others adhered slightly to adjoining tissues. The dithyridium 
has a milk-white body, varying in length from 1.5 to 2.5 mm. It is 
sometimes as broad as long and sometimes much longer than broad. 
An invaginated cestode scolex is present. 

manson's eye worm 

At least 38 species of nematode worms have been reported as 
parasitic in the eyes of birds throughout the world. However, only 
one, Oxyspirura mansoni, is known to affect com- 
mon domesticated birds. This has been found in 

fowls and peafowls. Ransom has reported upon its 

' • j-i, TT -4- J 04. J. J j-i, Fig. 34. Manson's 

presence m the United states, and upon the preva- gyg ■worm (Ox- 

lence of nematodes in wild birds. yspirura man- 

General description. The parasite known as ^^^oJq and female 
Oxyspii'ura mansoni or Filaria mansoni or Spi- below. Natural 
roptera emmerzii is a small white, thread-like ^^^^' ^ an^om) 
worm slightly over half an inch in length and about as thick as a fine 
sewing needle. It is thickest in the middle and tapers toward the 
ends. The number present in the eyes may vary from a few located 
beneath the nictitating membrane to as many as 200. 

Symptoms. In some cases the worms are present in the eyes 
without causing apparent inconvenience. In more severe infesta- 
tion, symptoms of irritation become evident. The affected bird ap- 
pears uneasy and scratches the eyes. The latter show acute inflam- 
mation with abundant lachrymation. Subsequently white cheesy 
exudate collects within the conjunctiva and upon the edges of the 
lids, causing them to adhere together. The inflammation extends 
to the tissues surrounding the eye and to the infra ocular sinuses. 
Eventually the whole eyeball becomes affected, with consequent de- 
struction of the organ. Catarrhal changes also involve the nasal 
cavities. In severe cases the subject dies. 

Treatment. The first requisite to successful treatment consists 
in removing the worms. This may be done by the use of forceps or 
by irrigating the eyes with some solution such as bicarbonate of 
soda or a two per cent solution of creolin. When the worms are 
partially dislodged by the fluid, they may be entirely removed with 
a soft cloth. The inflammation may be alleviated by instilling into 



202 



DISEASES OF DOMESTICATED BIRDS 



the eyes a few drops of saturated solution of boric acid. Ransom 
recommends anointing the eyes with a mixture of lard 9 parts and 
iodoform, 1 part or with carbolized vaseline. 

Life history of the worm. Very little is known of the life his- 
tory of the parasite. It seems probable that the embryos pass a 
portion of their existence either free or in a secondary host. The 
reports of the presence of the worm in chickens are, so far as known, 
limited to sea coast regions. This suggests the possibility that some 
conditions peculiar to the sea coast are necessary to the development 
of the parasite. 

LEECHES IN THE EYE 

One incomplete report exists of the occurrence of leeches in the 
eyes of geese in Ireland. Intense irritation of the eye occurred, 
with symptoms of severe pain. The birds had access to a pond 
teeming with leeches. 




Fig. 3.5. Lamin- 
osioptes cysti- 
cola. Male, 

ventral aspect. 
Enlarged 200 
times. (Rail- 
liet) 



MITES PARASITIC IN CONNECTIVE TISSUE 

Laminosioptes cysticola, accord- 
ing to Neumann, is a mite occur- 
ring in gallinaceous birds such as 
fowls, pheasants and turkeys. The 
parasites live on the surface and 
in the thickness of the skin caus- 
ing the formation of scurf. They 
are encountered rarely except in 
the subcutaneous tissue especially 
in the places where it is very loose, 
such as the flanks, the vent, on the 
thighs, the breast and the neck. 
They are able to penetrate the deep 
connective tissue. Microscopic ex- 
amination of fragments of subcu- 
taneous connective tissue permits 
all phases of their development to 
be observed. When they die, the 
carcass acts as a foreign body and 
causes the formation of a miliary 
nodule about it. This promptly 
undergoes calcareous infiltration. 
On treating these nodules with 




Fig. 36. Laminosi- 
optes cysticola. 
Ovigerous female, 
ventral aspect. 

Enlarged 2 
times. (Railliet) 



INTERNAL PARASITES 203 

acidulated water, the remnants of the parasite may be recovered. 
The nodules are yellowish in color, oval in shape and may become as 
large as 1 mm. in diameter. They may be very numerous in an 
individual and are very common in old cachectic birds. These para- 
sites are not injurious to health except perhaps when they are present 
in excessive numbers. 

Two other connective tissue parasites occur in the pigeon. A 
feather mite, Falculifer rostratus, spends a portion of its life cycle in 
the subcutaneous connective tissue. Filaria clava is located in the 
subcutaneous connective tissue of the pigeon. Neither have any 
effect upon the health of the host. 

TRYPANOSOMIASIS OF BIRDS 

The blood of a very large number of wild birds is infested with 
trypanosomes which apparently do not exert much pathogenic effect. 
Gray lists nine species of these parasites occurring in birds. Among 
domesticated birds, they have been observed in the fowl and pigeon. 

FILARIA IN THE BLOOD 

Filaria anatis has been observed in the heart of a duck. Embryos 
of filaria have been observed in the blood of a pigeon. 

PARASITE OF AVIAN MALARIA 

Symptoms. The parasite of Danielewsky, n<rmoproteus danie- 
lewskyi has also been designated Hcemomoeha danielewskyi, Halter- 
idium danielewshyi and Plasmodium danielewskyi. 

General nature. The parasite of avian malaria, one of the 
hematozoa of birds, has many points of resemblance with the parasite 
of malaria of man. 

Distribution. The parasite occurs in a large number of wild 
birds. Cardamatis examined the blood of 38 species of birds in 
Greece, including 936 specimens. Of 724 local birds, 21.79 per cent 
were affected. Of 212 migratory birds, 32.07 per cent were infected. 
The domestic pigeon is the only domesticated bird reported as in- 
fested by the parasite. Aragao refers to the parasite of the pigeon 
as a separate species, H. columhce. 

Symptoms in wild birds. Cardamatis observes that birds in- 
tensively infected appear less lively, the plumage is dull and emacia- 
tion causes them to appear smaller. 



204 



DISEASES OF DOMESTICATED BIEDS 



Lesions in wild birds. The organs according to Cardamatis, 
show characteristic alterations resembling those caused by malaria in 
man. The blood of sick birds is sometimes watery, less abundant 
than normal, pale, and coagulates slowly. The spleen is colored like 




Fig. 37. Hcemoproteus danieleicskij in blood of the pigeon under different as- 
pects. 1, 2, red blood corpuscles containing small parasites; 3, red blood 
corpuscle containing a large female parasite; 4, red blood corpuscle contain- 
ing a large male parasite; 5, corpuscle with a female and a male parasite; 
6, parasite after rupture of the corpuscle which had contained it (The nu- 
cleus of the cell is still seen coupled with the parasite) ; 7, male parasite 
with four flagella; 8, female parasite into which a flagellum is penetrating 
(fecundation) ; 9, a free flagellum. Enlarged 1500 diameters. (Neumann) 

chocolate or darker and is always swollen to twice the normal size. 
This writer found turtle doves and lanners most susceptible. Iturbe 
and Gonzales note that while the hematozoa frequently have no ef- 
fect upon the host, the mortality may reach 90 per cent in Myiozetes 
texensis, Chlorophonia prettii and Sycalis flaveola. 

Transmission. Aragao observes that the natural transmitters of 
H. columbce in Brazil are Lynchia livicolor and Microlynchia persilla; 
in Algeria, L. maura; in the Transvaal, L. capensis. Direct inocula- 
tion from pigeon to pigeon fails. 



LEUCOCYTOZOA 

Leucocytozoa are blood parasites which so modify the appearance 
of the host cell that the identity of the latter is in controversy. • Ean- 
tham inclines to the view that small mononuclear leucocytes are the 
cells invaded. Leucocytozoa have been observed in a large number 
of wild and domesticated birds. Among the latter, fowls, pigeons, 
ducks, ostriches and turkeys are known to be infested. In general 
they are of slight importance as disease producers. 



INTERNAL PARASITES 205 

leucocytozoGn infection in ducks 

Wickware observed an outbreak of disease among young ducks 
under circumstances that led him to suspect that leucocytozoa were 
responsible. Bacteria could not be excluded as a cause, for it was 
not possible to seed culture media. 

Symptoms. The affection runs a rapid and fatal course, with 
few symptoms to indicate its onset. Impaired appetite is first no- 
ticed in that the birds refuse to respond to the call for feeding. In 
some cases ducks succumb during the first paroxysm, while others 
survive a series of exacerbations. Affected ducks lie in a semi- 
comatose condition with the neck bent backwards and the head resting 
upon the dorsal portion of the spinal column. When roused from 
this stupor the bird experiences a period of intense excitement during 
which remarkable movements are made. The head is held in various 
positions, or describes circles in the air, or at other times swings to 
and fro. In some cases the neck is completely turned on itself with 
the head resting on the ground in an upright position. The power 
of equilibrium is lost and the bird turns over backwards until ex- 
hausted. In recovered birds, there is lameness and consequent 
difiiculty of locomotion. Purulent ophthalmia with adherent lids 
is a quite constant symptom. The mortality is about 65 to 70 per 
cent. 

Etiology. The leucocytozoon present in the blood of ducks in 
two outbreaks of disease is designated by Wickware as Leucocytozoon 
anatis. The shape of the parasites is fairly uniform although there 
appears to be considerable pleomorphism in the gamete forms. The 
predominant type is a spindle shaped organism 35 microns to 60 
microns in length by 10 microns in width, showing an oval elongated 
or irregularly shaped nucleus, with dark chromatic band extending 
along one border. With Giemsa, the nucleus stains a dark blue and 
has a granular appearance. In the center there may be observed a 
small chromatin staining body varying slightly in shape. The 
cytoplasm appears almost transparent or at most stains a faint pink. 
At each end it terminates in an acute angle. Considerable varia- 
tion occurs in the staining characteristics of the mature forms. 

Morbid anatomy. Other than acute hemorrhagic inflammation 
of the large intestine behind the ceca, no abnoraiality of the visceral 
organs was observed. The blood in all cases of infection showed an 
increase of eosinophiles, besides the leucocytozoa. 



206 DISEASES OF DOMESTICATED BIEDS 



REFERENCES 

1. Aragao. Pesquizas sobre o " Haemoproteus cohimbse." Brazil-Med- 
ico. 4 et 11 Nov., 1916. Abs. in Bull de I' Inst. Pasteur, T. 15, p. 300. 

2. Cardamatis. Le paliidisme des oiseaux on Grece. Etude biologique 
et histologique du parasite de Danielewsky. Centralhl. f. BaJcteriol. 
{Etc.), 1 Alt. Orig., Bd. 59, 1909, S. 351. 

3. Ciurea. Nematoden aus dem Pharynx und Osophagns des Haushuhn. 
Ztschr. f. InfeUionsl-r. d. Haustiere., Bd. 15, 1914, S. 49. 

4. Freese. Ueber die durch den Strongylus nodularis hervorgerufene 
Magenwurmseucbe bei jungen Giinsen und die durch Trichosomen 
CTrichosoma retusem Railliet) verursachte Darmwurmseuche. Deutsche 
tierdrztl. Wchnschr., Bd. 16, 1908, S. 713. 

5. Gage and Opperman. A tapeworm disease of fowls. Md. Agr. Exp. 
Sta. Bull. 1S9, 1909. 

6. Gutberlet. Studies on the transmission and prevention of cestode in- 
fection in chickens. J. Am. Yet. M. Ass., Vol. 2, 1916, p. 218. 

7. Hadley. The role of the flagellated protozoa in infective processes 
of the intestines and liver. Bhode Island Agr. Exp. Sta. Bull. 166. 

8. Hadley. The avenue and development of tissue-infection in intes- 
tinal trichomoniasis. Bhode Island Agr. Exp. Sta. Bull. 168. 

9. Hadley. The case of trichomonas. Amer. Nat., Vol. 51, 1917, p. 209. 

10. Hadley. The part played by the goblet cells in protozoan infections 
of the intestinal tract. J. Med. Research, Vol. 36, 1917, p. 79. 

11. Herms and Beach. Bound worms in poultry-life history and con- 
trol. Univ. Cal. Agr. Exp. Sta. Circ. 150. 

12. Iturbe and Gonzales. El paludismo de las aves en Venezuela. Lab. 
du Dr. Iturhe, Caracas, 1916. 

13. Martin et Daille. Sur une blastomycosis Hepatique de 1' Oie. 
Bev. Vet., T. 7, 1912, v. 129. 

14. Martin and Robertson. Further observations on the cfecal para- 
sites of fowls, with some reference to the rectal fauna of other verte- 
brates. Quart. J. of Micr. Sc, Vol. 57, 1912, p. 53. 

15. Moore. A nodular tseniasis in fowls. U. S. Dep. Agr. Bureau Ani- 
mal Indust. Circ. 3. 

16. Neumann. Parasites et maladies parasitaires des oiseaux domes- 
tiques. Paris: Asselin et Houzeau. 1909. 

17. Ransom. Manson's eye worm in chickens. U. S. Dep. Agr. Bureau 
Animal Indust. Bull. 60. 

18. Ransom. A new nematode (Gongylenoma ingluvicola) parasitic in 
the crop of chickens. U. S. Dep. Agr. Bureau Animal Indust. Circ. 6Jf. 

19. Ransom. The tapeworms of American chickens and turkeys. U. S. 
Dep. Agr. Bureau Animal Indust. Circ. 85. 

20. Robertson. Notes on ostrich parasites. Agr. Jour. Cape of Good 
Hope, Vol. 33, 1908, p. 583. 

21. Stiles. Report upon the present knowledge of the tapeworms of 
poultry. TJ. S. Dep. Agr. Bureau Animal Indust. Bull. 12. 

22. Theobald. The gape worm and the white intestinal worms of poul- 
try. Jour. Bd. Agr., Vol. 6, 1899, p. 157. 



INTERNAL PARASITES 207 

23. Theobald. Parasitic diseases of poultry. London : Gurney & Jack- 
son, 1896.. 

24. Walker. A short note on the occurrence of a leucocytozoon infec- 
tion. Host the ostrich. Union of So. Africa. Dep. Agr. Ann. Rpts. Dir. 
Vet. Res., 2, 1912, p. 384. 

25. Weinzirl. Trichomoniasis of chicks : a new and highly fatal dis- 
ease. J. Bad., Vol. 2, 1917, p. 441. 

26. Wickware. Intestinal parasites of poultry, their prevention, and 
treatment. Dominion of Canada, Dep. of Agr. Health of Animals Branch. 
Bull. 25, 1917. 

27. Wickware. Is Leucocytozoon anatis the cause of a new disease in 
ducks? Dep. Agr. Canada. Rept. Vet. Dir. Gen., 1915, p. 95. 

28. Wilcox. The internal chicken mite. Montana Agr. Exp. Sta. Bull. 
S2, p. 30. (Bibliography.) 

29. Williams. The air sac mite of the fowl. Am. Vet. Rev., Vol. 22, 
1898, p. 8. 



CHAPTER XVII 

EXTERNAL PARASITES 
LICE 

General nature. Bird lice are wingless parasitic insects with 
mouth parts adapted to biting, not sucking. Lice in general perma- 
nently infest the host bird except when moving to other individuals. 
Opportunity exists for this migration on the roost, the nest, during 
copulation or while a hen is hovering chickens. Occasionally lice 
which are normally parasitic for the hen, guinea-fowl or turkey 
will be found on another species in close contact. 

Lice feed on epidermal products such as feathers, 
scales and the skin itself. Blood dried on the skin 
may be eaten but lice are not blood suckers. 

Injury caused by lice. Their presence causes 
pruritis set up by their claws and mouth parts. 
Excessive infestation undoubtedly is a serious hin- 
drance to normal gTowth and development. Brood 
hens are annoyed in some cases to such an extent 
that there is interference with incubation. In the 
Fig. 38. Head Southern States, there is a heavy mortality among 
A^ew" Greatly chicks liatched by hens after April 1, which may be 
enlarged. (Bish- attributed to the heavy infestation by lice. Bishopp 
opp and Woo ) ^^^ Wood regard symptoms of lice infestation as 
consisting of droopiness, lowered wings and ruffled feathers. In 
gro^vn fowls heavy infestation may be tolerated without causing ill 
eifect. In other cases there is reduction in egg yield and loss of 
weight. 

Species of lice. More than 40 species of lice occur on domesti- 
cated birds. Some species are restricted to one host, while others 
infest several different host species. Bishopp and Wood state that 
seven species are very commonly found on chickens in the United 
States, four or five on pigeons, two or three each on geese and ducks, 
three on turkeys and several each on guinea fowl and peafowl. 
Tliese are: On chickens, the head louse (Lipeurus heterographus ) , 
the body louse (Menopon hiseriatum) , the shaft louse (Menopon 
pallidum), the wing louse (Lipeurus variabilis), the fluff louse 

208 




EXTERNAL PARASITES 



209 



(Ooniocoies holocjaster) , the large hen louse (Goniocotes ahdomi- 
nalis) , the brown chicken louse (Goniodes dissimilis) ; on turkeys, 
the large turkey louse (Goniodes stylifer) and the slender tur- 
key louse (Lipeurus meleagridis). The common body louse and 
the shaft louse of chickens sometimes are found on the turkey. 
On ducks Docopfiorus icterodes and Lipeurus temporalis are com- 
mon; on geese a variety of D. icterodes; on pigeons the slender 
pigeon louse (Lipeurus haculus) and the broad pigeon louse (Goni- 
ocotes coynpar) cause most of the harm from lice. 

Keumann lists 6 species as occurring on the pheasant as follows: 
Lipeurus variabilis, Goniodes colcliicus, G. truncatus, Goniocotes 
chrysoceplialus, Menopon productum, and M. hiseriatum; on the pea- 
fowl, Goniodes falcicornis, G. parviceps, 
Goniocotes rectangulatus and Menopon 
phceostomum; on the guinea-fowl, Lipeurus 
numidce, Goniodes nwnidianus, Goniocotes 
rectayigulatus, Menopon numidce and Lipeu- 
rus variahile of the fowl. In addition to 
the two species listed by Bishopp and Wood 
as important lice on the pigeon in the United 
States, ISTeumann mentions Goniodes minor, 
G. damicomis, Menopon gigantemn, M. 
longicephaJum, Liotheum longicaudum and 
M. hiseriatum of fowls as occurring on 
pigeons ; on geese, Lipeurus crassicomis, L. 
anseris, Trinoton anseris and T. lituratum; on ducks, L. anatis, T. 
luridum and Menopon ohscurum; on swans, Ornithonomus cygiii, 
Philopterus cygni and Trinoton anseris of the goose. 

The terms head louse, body louse, wing louse, etc., as applied to 
the lice of fowls indicate where the various species are found in 
greatest numbers and where their structure best adapts them to live. 
Thus the head louse exhibits a preference for the head but is occa- 
sionally found on the feathers of the wings. Some lice are adapted 
to live on the skin only, while others occur on the feathers as much 
as an inch from the skin. 

Life history. In general, lice spend their whole life on one host. 
All the finer details of the life history of lice have not been worked 
out. The eggs, attached to the feathers are commonly known as nits. 
In the case of the head louse they hatch in four or five days. The 
young, after molting the skin several times, reach the adult stage in 
17 to 20 days. 




Fig. 39. Eggs of the head 
louse (Lipeurus hetero- 
firaphi(s) on feather. 
Greatly enlarged. (Bish- 
opp and Wood) 




210 DISEASES OF DOMESTICATED BIEDS 

Combating lice. Owing to the habit of lice of 
remaining upon the host, the most direct method of 
combating them consists of the application of an in- 
secticide to the bird, 

Bishopp and Wood favor starting a campaign 
against lice in the late summer or early fall. The 
weather conditions are favorable and the amount of 
stock to be treated is the lowest of any time in the 
year. There is no reason to prevent a flock from 
being entirely freed from lice and kept free. 

These writers conclude that the commercial grade 

^^?' ^^', i,r ^^^^ of sodium fluorid is the most satisfactory agent to 
louse {Menopon . . . , ,. 

his eriatum) : use agamst lice. It kills lice m all stages including 

Male, top view, {j^q^q hatchine; subsequent to its application. They 
Greatly enlarged. ^ . ^ „,/ ^ t ^ • i 

(Bishopp and apply the agent m two ways. When applied m the 

^"^'^^ powdered form, the bird is held in a pan to catch 

superfluous powder. They apply one pinch on the head, one on the 
neck, two on the back, one on the breast, one below the vent, one on 
the tail, one on either thigh and one scattered on the inner side of 
each wing when spread. They recommend this method of applica- 
tion for newly hatched birds and sick birds exclusively. The action 
of the powdered sodium fluorid is comparatively slow, but it remains 
on the bird, and in four or five days all lice will disappear. The 
dust is somewhat irritating to the air passages and the operator 
should wear a dust protector over the mouth and nostrils. The 
powder causes a transitory effect only on the air passages of the 
treated birds. The method costs about $1.25 per hundred fowls, 
calculating the man's time at 20 cents per hour. 

Applying the agent in solution by dipping has the advantage in 
reducing cost of materials and is more rapidly done, without discom- 
fort to the operator. Furthermore, the lice die very promptly after 
being touched by the fluid. The first requisite is a warm, sunny day 
so that the fowls will dry quickly. The solution is prepared in a tub 
in the proportion of three-fourths to one ounce of commercial sodium 
fiuorid to each gallon of tepid water. In dipping the birds, the wings 
are held over the back with the left hand while the bird is sub- 
merged in the solution with the head out. The feathers are thor- 
oughly ruffled with the right hand to secure penetration of the fluid 
to the skin all over the body. The head is ducked once or twice, the 
bird is drained a few seconds and is released. The work of dipping 
should be stopped sufficiently early in the afternoon to permit the 



EXTEENAL PARASITES 



211 



j^:^:<v^f 




Fig. 41. Mass 
body louse eggs 
attached to 
feather. Greatly 
enlarged. (Bish- 
opp and Wood ) 



birds to become dry before night. By the dipping method the cost 
for material is 58 cents per hundred birds. For material and labor 
both, it is 71 cents. 

Bishopp and Wood note that several other agents are effective in 
destroying lice, but are more expensive than so- 
dium fluorid. Flowers of sulphur applied with a 
dust can in an amount of about 6 pounds per hun- 
dred fowls is effective in about four days. Dip- 
ping fowls in a solution of 1 ounce of laundry soap 
to a gallon of water, rejDeated in ten days is ef- 
fective. 

Herrick strongly recommends the Cornell or 
Lowry dusting powder made as follows : Two and 
one-half pounds of plaster of Paris is spread in a 
shallow pan or tray. One-fourth pint of crude 
carbolic acid is poured into a cup, and into this is 
poured three-fourths pint of gasoline. The mix- 
ture of acid and gasoline is poured over the plas- 
ter of Paris and thoroughly mixed. It is then rubbed through a 
wire window screen on a piece of paper and allowed to stand for 
from one and one-half to two hours or until thoroughly dry. It 
must not be placed near a flame or any heat. The powder should be 
kept in a closed can or jar, where it will retain its strength for a long 
time. The powder is applied by means of 
an ordinary sifter or with the fingers. It is 
worked in among the feathers about the vent, 
in the fluff, and under the wdngs. Two and 
perhaps three applications should be made. A 
small pinch of the powder is sufiicient for a 
fowl. The rooster should receive especial care 
in being kept free from lice, as he is an im- 
portant factor in spreading the parasites. 

The expense of this treatment including la- 
bor should not exceed 32 cents per hundred 
fowls. 

Fig. 42. Large hen louse. rpj^^ effectiveness of this method of dusting 
(Gomiocotes abdonn- ,.,«,., n i • • i 

nalis): Male, top birds for lice has been called into question by 
view. Greatly en- several observers. 

larged. ( Herrick ) t -« r ^ ^ i • 

Lamson and Manter recommend the appli- 
cation of a dilution of either mercurial ointment or blue ointment. 
Mercurial ointment was considered cheaper when judged on the basis 




212 DISEASES OF DOMESTICATED BIRDS 

of content of metallic mercury. The mercurial ointment is mixed 
with one or two parts of vaseline. One ounce is sufficient to treat 
about seventy-five hens. In the case of chickens it is desirable to 
place a piece of ointment the size of a pea, under the wings or around 
the vent. In older stock the best place is on the skin just beneath 
the vent. The treatment seems to remain effective for some time, 
so that lice hatching after the application are also killed. It is not 
clear that the use of mercurial ointment is cheaper or more effective 
than sodium fluorid. Bishopp and Wood find that when used as 
recommended, the mercurial product has little effect upon head and 
wing lice. Used in larger amount it is more expensive and injurious. 

The dust bath constitutes the natural defense of fowls against lice 
and should be considered in connection with the measures against 
them. It is desirable that the box be located in the sunlight, and if 
covered, will prevent widespread dissemination of dust in the poultry 
house. The finer and lighter the material available, the better. 
Fine siftings from coal ashes is a desirable addition to the dust, as 
also are snuff, sulphur and dry slaked lime. The dust bath, while 
desirable, cannot be depended upon to the exckision of more aggres- 
sive measures. It has only a temporary effect upon the numbers 
of lice on the fowls. Some birds seldom or never use the dust box. 

In a flock infested with lice special care must be taken to free the 
sitting hen from these parasites and to protect young chicks in like 
manner. 

THE BIRD FLEA 

The common bird flea, Pulex avium., attacks a large number of 
species of birds including fowls and pigeons. The parasite is pro- 
vided with piercing mouth parts with which it penetrates the skin and 
extracts blood. The irritation produced by the fleas causes pruritis 
and loss of rest. 

Life history. The eggs are laid in hens' nests or on manure on 

the floor of the poultry house. 
These nits after a week or ten days 
hatch into white larvae which are 
nearly a quarter of an inch in 

Fig. 43. Larva of hen flea enlarged length. The larval stage lasts from 
20 times. (Railhet) *=• , . ^^, ^ _ 

ten days to three weeks, depend- 
ing upon the temperature. The fully developed larva becomes 
secreted in some crevice and spins itself a cocoon. In this structure 
the larva develops into the adult stage during a period varying from 




EXTERNAL PARASITES 213 

ten to twenty-one days. Fleas are temporary rather than permanent 
parasites, and are nocturnal feeders. During the day they hide in 
various protected places about the poultry house. Sitting hens suffer 
severely from their attacks. 

Combating fleas. Kepression of fleas is accomplished by the 
spraying necessary for combating mites. The use of whitewash con- 
taining a small percentage of kerosene oil destroys larvae, fills up 
lurking places and drives adults away if it does not kill them. Wood 
shavings is a desirable material for making nests, as it is repellent 
to fleas. Simple construction of interior fixtures to facilitate re- 
moval and cleaning is as necessary in connection with combating 
fleas as in combating mites. 

CHIGOE 

A second true flea, the chigoe, Sarcopsylla gallinacea, causes in- 
jury in quite a different manner. The male penetrates the skin, 
while the female becomes fixed to the skin so it is not detached 
quickly. Fowls, ducks and various animals are subject to attack. 
The parasite is found in great numbers about the eyes and neck- 
It is widely distributed, having been reported as occurring in Ceylon- 
Florida, South Carolina, Italy, Turkestan and various portions o£ 
Africa. 

FLIES PARASITIC UPON PIGEONS 

A fly, Oi'nithomyia avicularia, is parasitic upon a number of wild 
birds and has been reported as occurring on pigeons in France. It 
moves between the feathers and draws blood from the host. Li/nchia 
rnaura is a closely related species parasitic upon pigeons in Sicily 
and Algeria. These flies are especially abundant upon squabs before 
the plumage has developed. Their attacks cause emaciation and 
sometimes also a fatal anemia. Sitting birds are disturbed by 
the parasites and make quick movements which may result in break- 
ing the eggs. Sometimes the birds are so tormented that they 
abandon the dovecote. Sergent reports this fly as the secondary host 
of the blood parasite Hcemoproteus danielewsJcyi. L. capensis has 
been reported as parasitic upon pigeons in Teneriff. 

BED BUGS 

The common bed bug Cimex (Acanthia) ledularia occasionally in- 
fests fowls and pigeons at night for the purpose of sucking blood. 
During the daytime they inhabit cracks and sheltered places about 
the poultry house. 



214 



DISEASES OF DOMESTICATED BIEDS 




NEST BUGS 

The nest bug or dovecote bug Cimex (Acan- 
thia) columbara is a species closely related to 
the bed bug and which also attacks pigeons and 
fowls. Sitting hens suffer severely. Both this 
species and bed bugs are held in check by the 
routine measures recommended in combating 
mites. C. inodorus occurs in Mexico, ]^ew 
Mexico and Texas. 



Fig. 44. 
bug. A, 
size; B, 
(Railliet) 



LARVAL BEETLES ATTACKING HENS AND PIGEONS 

Tenebrio molitor is a beetle the larvae of 
which have been reported as attacking sitting 
Dovecote j^eus and pigeons. Pigeons have been reported 
enlarged, ^s Subject to the attack of larvse of Dermestes 
lardarius and other larvas of the genus Necro- 
phorus and genus Silpha. These coleopterous larvse develop in the 
manure of the dovecote, attack the skin of the squabs on the neck and 
abdomen and even the superficial muscles. The wounds become in- 
fested with fly maggots and are frequently fatal. The presence of 
the larvse may be prevented by cleanliness. Wounds may be treated 
with antiseptics. 

RED MITES 



Synonyms. Poultry mite, chicken mite, roost mite. 

Hosts. Pigeons, fowls, turkeys, pheasants, domesticated mam- 
mals and man are subject to attack by the parasites. 

General nature. The common poultry mite, Dermanyssus gal- 
lincc in general, infests birds only temporarily while they are on 
the roost. It is a blood sucker, and be- 
sides causing loss of blood, induces intense 
irritation. 

Individual mites are barely visible to 

the unaided eye, but owing to the habit of 

collecting in masses, thev are easily de- 

, '^ . n 1 ■ 1 ' -xi Fig. 45. Egg of the 

tected, especially when engorged with chicken mite (Dermamjs- 

blood and colored red. When not en- «"« gniiincc) . Greatly 
, , . , enlarged. (Bishopp and 

gorged, they are gray in color. Wood) 





EXTEKNAL PAKASITES 



215 



The parasite is widely distributed throughout the world. Its 
depredations are more serious in warmer countries because of favor- 
able climatic conditions. 

Habits. During the daytime the mites collect in cracks, or under 
droppings and rubbish. They make their way at night to the birds 
on the roost where they cause annoyance 
while engorging with blood. Occasion- 
ally mites will attack hens on the nest 
during the daytime. When engorged, 
the mite leaves the bird. Some mites 
that fail to become engorged the same 
night they gain access to the bird, will 
remain on the host during the following 
day or so. Thus hens have been found 
to carry as many as a hundred mites dur- 
ing the daytime. Eggs are laid in the 
places sheltering the mites, and hatch in 
two days or more depending upon the 
temperature. The larvae hatching from 
the eggs shed their skins in about two 
days and become nymphs. After several 
engorgements and molts, the parasite reaches maturity. The whole 
life cycle is complete in a week. The parasites are not active in cold 
weather. In the absence of poultry, mites will remain alive in in- 
fested houses for four or five months. Moisture seems to favor their 
longevity. 

Injury caused by mites. Excessive mite infestation has been 
held responsible for increase in cost of maintenance, decrease of 




Fig. 4G. First nymphal stage 
of the chicken mite, unfed. 
Greatly enlarged. (Bishopp 
and Wood) 



egg laying and general unthriftiness. 



Sitting 



hens have been 
The attack of the 



driven by the irritation, to abandon the nest 
mites rarely leaves a trace on the skin. 

Combating mites. In combating the pest, it is recommended 
that all interior fittings be removed so as to minimize the number of 
cracks in which mites could escape the action of the spray. If the 
house is of the older type, with built-in accessories such as perches and 
nests, everything should be torn out leaving merely the four bare 
walls. The whole house should be thoroughly swept and all rubbish 
removed. Kerosene oil, or kerosene emulsion constitute suitable 
agents for killing mites. One of these agents should be applied with 
a spray pump, particular care being taken to force the fluid into 
cracks. Since it is quite likely that some mites and eggs will 



216 



DISEASES OF DOMESTICATED BIEDS 




escape being hit by the fluid, it is necessary to repeat the applica- 
tion in a week and perhaps a third time may be necessary. 

Bishopp and Wood recommend crude petroleum as the most ef- 
fective agent and one that retains its killing power for weeks. To 

improve its spraying quality it 
may be thinned with one part of 
kerosene to four parts of crude 
oil. They likewise find arseni- 
cal dip such as used for dipping 
cattle to be fairly satisfactory in 
killing mites when applied sev- 
eral times. 

Repp recommends preparing 
kerosene emulsion as follows : 
One-half pound of laundry soap 
or whale-oil soap is shaved fine 
and dissolved in 1 gallon of 
water. The soap is best dis- 
solved if the water is nearly 
or quite at the boiling point. 
When the soap is dissolved and 
the water is hot it is removed from the fire, 2 gallons of kerosene 
oil is added, and the mixture is agi- 
tated or churned violently until 
emulsion is formed. The best way 
to produce the emulsion is to pump 
the liquid back into the same con- 
tainer through the pump until the 
mixture becomes creamy. To 
make a ten per cent emulsion, 17 
gallons of water are added to the 3 
gallons of stock mixture ; to make a 
fifteen per cent emulsion, 10^ gal- 
lons of water are added to the 3 
gallons of stock mixture. 

Subsequent to spraying with 
kerosene emulsion it is desirable to 
dust the entire interior of the Fig. 48. Female chicken tick after 
houses with a mixture of air slaked feeding Greatly enlarged. (Bish- 

opp and Wood) 
lime, 3 parts and sulphur, 1 part, 

A further measure against mites consists in painting the perches 



Fig. 47. Female chicken mite before 
feeding, greatly enlarged. Mouth 
parts at right highly magnified. 
(Bishopp and Wood) 




EXTERNAL PARASITES 217 

with a mixture consisting of three parts of kerosene to one part of 
crude carbolic acid. 

The presence of all sorts of rubbish affords lurking places for 
mites and decaying matter such as broken eggs attracts them par- 
ticularly. 

When fowls are moved to fresh quarters from infested quarters it 
is desirable that they be left for three days in a pen so that all mites 
will have opportunity to leave the birds. 

Mites are disseminated not only by live birds bearing them, but 
by all such articles as crates and other objects that have been in 
poultry li(iuses. The introduction of mites by pigeons or sparrows is 
quite possible. 

Infestation of man. People in close contact with infested hen 
roosts are liable to be attacked by the mites. They cause an 
ephemeral itching lesion on the back of the hand and other exposed 
portions of the body. However, they may affect any portion of the 
body. 

Occurrence on horses. When poultry roosting quarters are near 
or in the stable, horses are subject to infestation. They cause severe 
pruritis during the night. The mites cause the formation of small 
vesicles single and grouped together. These vesicles are rubbed off, 
accompanied by depilation, but the areas soon become covered with 
new epithelium. This gives the skin a characteristic flea-bitten ap- 
pearance. To these changes are added others resulting from ex- 
cessive rubbing. 

Mites in the external ear. Mites have been observed in the 
outer ear of chickens and ducks. In the case of the latter, unusual 
movements of the head occurred. The mites were considered by the 
observer to be D. gallince but l^eumann expresses doubt concerning 
the identification. 

HARVEST MITES 

Harvest mites are first stage larvas of certain species of the genus 
Tromhidium. They are commonly known as chiggers, a name which 
is evidently a corruption of the term chigoe, used to designate a 
species of flea. The harvest mites attack a wide variety of hosts, 
including poultry. They attach themselves in groups to the skin 
beneath the wings and on the breast and neck. Their presence causes 
areas of severe irritation and suppuration. Young chickens are most 
susceptible and their death has been attributed to the result of the 
presence of the parasites. 

Mites occur in a wide variety of places such as in damp locations 



218 



DISEASES OF DOMESTICATED BIRDS 



along the borders of streams, in trees and shrubbery and on the 
borders of forests. 

In the United States they are most numerous in the South but are 
well distributed in Kansas, Indiana and Iowa. In England and 
Scotland they are known popularly as gooseberry bugs. 

Chickens should, so far as possible, be kept from ranging in areas 
known to be infested. Dusting the feathers with sulphur is useful 
in keeping the mites off. The application of sulphur ointment or 
kerosene and lard for killing the mites on the skin is recommended 
by Bishopp and Wood. Eroded areas may be treated antiseptically. 



SCALY LEG OR FOOT MANGE 

The mite designated Cnemiodocoptes mutans (Sarcoptes mutans) 
affects the legs of fowls below the tarsal joint. 
Other domesticated birds are affected more rarely. 
The first evidence of infestation consists of the ap- 
pearance of grayish white areas which gradually 
coalesce and thicken. The parasites burrow in the 
skin and set up cellular proliferation with exuda- 
tion. This thickens the skin and causes the natu- 
ral scales of the leg and toes to protrude. In an 
advanced case the skin is covered with thick gray- 
ish white crusts which appreciably increase the 




Fig. 49. Cnemio- 
docoptes {Sar- 
coptes) mutans. 
Male, dorsal as- 
pect enlarged 
100 times. (Neu- 
mann) 



size of the leg and toes, 
leg interferes with 
the motion of the 
joints. The skin is 
inflamed and raw. 
Examination of some 
of the crusts will re- 
veal the presence of mites. Itching is 
present as indicated by the pecking of 
the lesion by the bird. In extremely 
advanced cases the bird may become 
lame, arthritis may develop, toes may 
be lost, and the bird may squat continu- 
ously. The infestation may be accom- 
panied by loss of condition and even 
cachexia terminated by death. 

Treatment.' The legs of the af- 
fected bird should be soaked in warm 
soapy water and be thoroughly cleaned 



The enlargement of the 




Fig. 50. Cnemiodocoptes (Sar- 
coptes) mutans, ovigerous 
female, dorsal aspect, en- 
larged 100 times. (Rail- 
liet) 



EXTERNAL PAEASITES 



219 



by scrubbing with a brush. The most effective remedy consists of 
the application of an ointment consisting- of one part of caraway oil 
and four parts of lard or of white vaseline. Another remedy con- 
sists of sulphur ointment made of 1 part of sulphur and nine parts 
of lard. Crude petroleum is effective. 
Plain kerosene oil sometimes employed is 
somewhat effective but will become smeared 
on the thighs as soon as the bird perches, and 
will blister the skin. The application of 
any remedial agent should be repeated. 

Prophylaxis. Removal of infected 
birds from the flock, and general disinfec- 
tion should be carried out immediately fol- 
lowing the discovery of the disease. 




DEPLU:ming scabies Fig. 51. Sarcoptes miitans. 

Ovigerous female. Dorsal 

The mite designated Cnemiodocoptes ^iew. Enlarged lOO times. 
(Sarcoptes) Icevis may occasion loss of 



[Railliet) 




Fig. 52. Cnemiodocoptes 
kevis, larva, ventral aspect, enlarged 
200 times. (Railliet) 



feathers in fowls, pigeons and 
pheasants during the spring and 
summer. It infests the portion 
of the quill that lies beneath the 
surface of the skin. The affecr 
tion usually appears first on 
some spot on the body, and pro- 
gresses gTadually to the neck, 
thighs and head, or the head and 
neck may be affected first. The 
frequency with which the back 
is first affected suggests that 
treading may be the principal 
means of dissemination. The 
large feathers of the wing and 
tail are not generally involved. 
The feathers are either shed 
entire, or the quills break off 
close to the level of the skin. 
Sometimes the stumps are 
(Sarcoptes) tracked and are surrounded bv 



epidermal scales 



220 DISEASES OF DOMESTICATED BIEDS 

The mites may be observed on the stumps of broken off quills or of 
feathers drawn from the border of the bald area. The irritation set 
up by the mites at the root of the feathers often causes the bird to 
pluck its feathers, or even sets up the habit of pulling the feathers 
of other birds. 

The skin is generally normal in appearance but occasionally ap- 
pears red and nodular. In severe cases, egg laying may be inter- 
fered with, and the birds become emaciated and die. 

Treatment. Treatment consists in the repeated application of 
essentially the same remedies as recommended for scaly leg, such as 
sulphur ointment. Salmon recommends two liquid preparations, a 
solution of balsam of Peru in alcohol (1:3) or a mixture of cre- 
olin, 1 dram; glycerine, 2 ounces; alcohol and water, % ounce each. 
Schleg's solution has been recommended for treatment. This con- 
sists of white arsenic and potassium carbonate each 1 dram, 3 pints 
of water and 3 pints of vinegar. 

OTHER MITES AFFECTING SKIN AND FEATHERS 

The mites Epidermoptes hilohatus and Epidermoptes bifurcatus 
have been found associated with a form of scabies affecting the skin. 
The beginning of the infestation is indicated by the appearance of 
fine yellowish scales which eventually develop into thickened brown- 
ish crusts. The parasite in question is frequently found on birds 
without the presence of lesions, so their presence in a lesion does 
not necessarily indicate that they are the cause. Treatment is 
similar to that suggested for scaly leg and depluming scabies. 

Other mites parasitic upon the skin and feathers and of less eco- 
nomic importance are listed by ^KTeumann as follows: On the fowl, 
PterolicJius obtusus. Derma glyphus minor^ D. elongatus, Megninia 
cuhitalis and M. colwnbce; on the turkey, Freyana chanayi, D. 
minor and M. cuhitalis; on the gTiinea-fowl, D. minor and D. vor 
rians; on the pheasant, P. ohtusus, P. uncinatus, M. cuhitalis and M. 
ginglymiira; on the peafowl, M. cuhitalis and M. ginglymura; on the 
pigeon, Falculifer rostratas, F. comutus, M. columhoe, Analges hijidus 
and Pterophagus strictus; on the goose and swan, F. anserina; on the 
duck, F. anatina and M. velata. 

OTHER PARASITIC MITES 

Mites parasitic in parts of the body other than the skin, occur 
in the nasal cavities, air sacs and connective tissue. These are dis- 
cussed in Chapter XVI. 



EXTEENAL PAKASITES 



221 



THE FOWL TICK 

Designations. Argas miniatus (A. Americanus). In various 
sections of the country the tick is designated by such popular names 
as tampan, blue bug or blood sucker. It has been referred to in 
the literature as the miana bug, from whence its specific name is 
derived. 

Hosts. Besides infesting fowls, it attacks turkeys, geese, pig- 
eons, ostriches and canaries. 




Fig. 53. Distribution of the fowl tick (Argas miniatus) in the United States. 
The large dots indicate localities where this tick has been collected by the 
Bureau of Entomology. The small dots show the normal distribution of 
the species within the United States. (Bishopp, Bureau of Entomology, 
U. S. Dept. Agr.) 

Injury produced. Bishopp summarizes the ways in which harm 
is done as follows: (1) Through death which may occur in poultry 
of all ages; (2) by the lowering of the vitality of the fowl so as to 
make it readily susceptible to disease; (3) by greatly reducing egg 
production; (4) by stunting the growth of chickens; and (5) by 
disturbing sitting hens. He further observes that death may be 
caused by gross infestation which drains the fowl of blood and 



222 DISEASES OF DOMESTICATED BIEDS 

produces intense irritation. This occurs when fowls are placed 
in coops which have not been occupied for months and which harbor 
hungry ticks. The infested birds appear paralyzed, the wings droop, 
the feathers are ruffled and appetite is lost. Death may occur within 
a few days after such heavy infestation, but if removed from the 
ticks, the birds will recover. 

The discussion of the subject of harm induced by tick infestation 
alone, is complicated by the fact that in most countries ticks are 
the carriers of spirochetosis, which is described on p. 135. In the 
absence of positive information as to whether or not the fowl 
ticks of this country carry spirochetosis, it is not possible to state 
just how much injury is done by ticks alone and how much by a 
disease transmitted by them. 

Distribution. The tick occurs in the western half of Texas and 
in a zone extending westward along the southern part of ISTew Mex- 
ico, Arizona and California. In the latter state the area extends 
northward along the western half of the state to a point slightly 
north of San Francisco. The area involved is indicated in Fig. 53. 
The distribution of the tick is thus seen to be confined to the warm 
portions of the arid and semi arid regions. In Texas it does not 
extend into areas where the annual rainfall exceeds 30 inches, which 
apparently prevents its extension into the eastern part of the state 
or eastward on the Gulf coast. Ticks may occasionally be shipped 
to northern states and find favorable conditions for a limited period. 
Elsewhere it occurs in Persia, Australia, Africa, South America, the 
West Indies, Mexico, Panama, India, Southern Russia and Rou- 
mania. 

Life history of the tick. The habits of the fowl ticks resemble 
those of bed bugs in that they are night feeders and spend the day in 
cracks and other protected places. Thus considerable injury may be 
inflicted to poultry without the knowledge of the owner. 

Eggs are deposited in secluded places and in the summer, hatch 
in from 10 to 15 days. In the winter the hatching period may ex- 
tend over three months. The young seed ticks soon make their way 
to a fowl and attach themselves to the skin of the breast, thighs, or 
elsewhere and engorge ' with blood. This period of feeding, during 
which the ticks are constantly attached to the fowl occupies from 
3% to 10 days. When it is completed the ticks drop from the host. 
Before feeding they are light gray in color but after feeding they 
become dark blue, and are about one-tenth of an inch in length. 

After 4 to 9 days the seed ticks undergo a molt and develop into 



EXTERNAL PARASITES 



223 




Fig. 54. Female fowl tick, as seen from above and beneath. Greatly enlarged. 

( Bishopp ) 

njinphs. The feeding habit of nymphs is different in that they re- 
main attached to the fowl for but a short time, at night. Nymphs 
molt two or three times, alternating with feeding periods before 
they become adults. The adult female tick is shown in Fig. 54. 

Contrary to the habits of many ticks the adult female does not 
die after depositing eggs. She may alternate feeding periods on 
the fowl with egg laying for three, four, or even seven times. 

Ticks display a remarkable ability to exist for long periods with- 
out food. Seed ticks have lived for 5% months without food, those 
in the first nymphal stage for nine months, those in the second 
nvmphal stage for 15 months, and adults for 2Y2 years. 

Combating ticks. The difficulties associated with eradicating 
ticks f ri ni a hen house are so great that in case the building is of 
little value, burning the structure would save time and trouble. 
Under conditions forbidding the employment of this extreme and 
effective measure, various substances may be sprayed on the wood- 
work and in the cracks. Crude Beaumont petroleum, carbolized 
whitewash, boiling water, strong kerosene emulsion and various creo- 
sote disinfectants have been recommended. Hot tar eliminates 
cracks and imprisons ticks. Ticks are very resistant to substances 
such as insect powder, kerosene and even fumigation with hydro- 



224 DISEASES OF DOMESTICATED BIKDS 

cyanic acid gas. 'No one application of any substance should be de- 
pended upon to kill all ticks, because of their ability to secrete them- 
selves, and because eggs secreted in cracks may escape destruction and 
hatch. 

In an infested flock, control measures must not be limited to the 
buildings, because first stage larvse remain attached to birds for 
days. To deal with these it may be quite sufficient to isolate the 
birds in other than the usual quarters, until the crop of larvae be- 
come engorged and drop off. An application of kerosene and lard 
to the breast and underneath the wings will destroy larvse. Dipping 
the birds in a 10 per cent solution of one of the coal tar dips is 
effective, but in general dipping is not recommended. 

Since ticks must crawl to the birds and do so only at night, suit- 
able isolation of the roosting perches is a valuable measure in pro- 
tecting birds. The construction of the roosting poles should be 
such as not to afford harboring places. The poles may be suspended 
from the ceiling by rods passing through cans of kerosene or sup- 
ported from beneath by a similar device. Such measures are ef- 
fective until the fluid becomes bridged over with dust or other ma- 
terial. 

Tick-proof construction. The secretive habits and resistance 
of ticks are such that the menace occasioned by them can effectively 
be met in the long run only by providing special building construc- 
tion. A poultry house built of painted corrugated iron or of gal- 
vanized iron over a framework of piping solves the tick problem. 
Cracks are reduced to a minimum and the extreme heat attained 
by the building during the daytime, is destructive to ticks. Fur- 
thermore, ticks may be destroyed by building a fire inside the build- 
ing, or by the use of a gasoline torch. Tick-proof perches and nests 
may be secured by setting the supports in vessels of kerosene. 

If it is not possible to provide all-metal construction, the wooden 
building should be put up with reference to avoiding cracks. In 
any event a shingle roof should be avoided. 

THE PIGEON TICK 

The pigeon tick (A.rgns rejiexus) occurring in Europe is a species 
closely related to the fowl tick. It is somewhat rare in England, 
Germany and other northern countries. Its habits are similar to 
the fowl tick. This species is a serious pest of pigeons, while fowls, 
ducks and geese are also attacked. 



EXTERNAL PARASITES 225 

REFERENCES 

1. Bishopp. The fowl tick. V. S. Dep. Agr. Bureau Entomol. Circ. 

"I- Bishopp and Wood. Mites and liee on poultry. V. S. Dep. A,r. 

TESlef'i W infesting tick. A,r. Ga. N. S. Wales, Vol. 7, 1896, 

"■fnaidub. Die Fnssoude des Gefl^els^ Ina„,^Djs. fj^ Ani,.al 

5. Hassall. Note on the chicken tick. U. b. uep. Jigr. 
Jndust 16th Ann. Bept., 1899, p. 496. 

1 Sit; ^J^^^^Jr:^^''c!::Jt^su. ... 

""T'Lamsfn anfLnter. So,ne lice and mites of the hen. Conn.elicul 
(Starrs) Agr. Exp. f »;J'»"- % ^ go. A^^traKa, Bull. U. W13. 
%"S":shnl'^ 'ThX^VX. Sou. cape of Goo, Hope, Vol. 23, 

'"?i\Z The chicken mite. ^?-^f/-/-;f ^^,f '{,r* i.»Wi<.. 
12. Robertson. Fowl tick experiments. J. i^ep. Agr. 

Vol. 12, 1905, p. 561. 



CHAPTEE XVIII 

INFECTIOUS DISEASES AND PARASITES OF THE OSTRICH 
ANTHKAX IIsT THE OSTRICH 

Characterization. Anthrax of the ostrich is an acute febrile in- 
fection caused by Bacterium anthracis. 

History. The disease was first reported by Henning in the Cape 
of Good Hope in 1894, and later by Kobertson. Theiler in 1912 also 
has described the disease. 

Etiology. Anthrax of mammals and of the ostrich is identical, 
the causative agent being B. anthracis. 

Pathogenicity. The disease is transmissible from ostrich to os- 
trich by inoculation with heart blood. It is also communicated from 
the ostrich to the sheep and goat by inoculation. A strain of anthrax 
occurring originally in cattle was inoculated into a sheep, with fatal 
result, and blood of this animal when inoculated into an ostrich 
caused death from the same disease. 

The susceptibility of man to anthrax constitutes an important 
reason for care in conducting autopsies. 

Symptoms. According to Theiler anthrax occurs in the ostrich 
in two forms : the peracute or apoplectic form and as anthrax fever. 
The peracute form attracts most notice for it invariably ends in 
death. In natural cases the birds are generally found dead in the 
morning, or in a moribund condition, comatose, paralyzed and ap- 
parently insensible. A bird may present the picture of health one 
moment and be dead of the disease a few minutes later. In such a 
sudden attack, the feathers become erect and the whole body is shaken 
with tremors. The bird staggers, lies do%\ai on the side and kicks con- 
vulsively, while the neck twists and untwists spasmodically. 

More chronic cases have been designated anthrax fever. The 
birds show symptoms of a general illness and do not feed well for a 
few days. The attack results in death, or more commonly in re- 
covery. 

Morbid anatomy. In the apoplectic cases the carcass is fre- 
quently in the best of condition and rigor mortis usually is absent. 
The blood escaping from the distended cutaneous and subcutaneous 
veins is usually dark in color and coagulates badly. 

226 



DISEASES AND PARASITES OF THE OSTRICH 227 

A smaller or greater amount of li(^uid is present in the pleuro- 
abdominal cavity and is occasionally colored red. 

Petecliise, eccliymoses or larger diffuse patches of hemorrhagic 
infiltration are observed on the ribs, on the pericardium, the per- 
itoneum and mesentery. Gelatinous infiltration of tissues also is 
observed. 

The pericardial fluid may be increased in amount. Hemorrhages 
and extensive hemorrhagic intiltraticms occur on the endocardium 
and epicardium. The blood in general is black in color, tarry in con- 
sistency and is either coagulated not at all or only partially. 

The lungs, jiroventriculus and gizzard are usually normal in ap- 
pearance. 

The small intestines usually show more or less intense infiltration 
with blood throughout the mucosa, which structure shows a uniform 
reddish discoloration. In some cases the hyperemia is irregularly 
distributed in patches and streaks throughout the length of the in- 
testines. The condition is visible from the serous surface of the in- 
testine. The acute inflammation may be found to be more pro- 
nounced in the colon where the mucous membrane is yet thicker. 
The surface of the mucosa is corroded, the submucosa is gelatinous 
and studded with hemorrhages, or softened and containing necrotic 
patches. The contents of the colon may include blood. 

The liver shows acute congestion, is enlarged and bluish in color. 
Blood escapes freely when the liver is incised. 

The spleen sometimes is normal in size and condition. However, 
usually it is enlarged and dark colored. The kidneys may be normal 
or congested, dark in color and friable in texture. 

Treatment. Theiler recommends carbolic acid diluted in water, 
in doses varying from one dram for a three months old bird to four 
drams for a two year old bird. 

Prevention. The preventive measures of isolation of sick and 
disinfection are very similar to those indicated in outbreaks of the 
disease among mammals. Carcasses preferably should be burned 
without opening or if this is impossible, should be buried in quick- 
lime at a good depth. All blood spilled at an autopsy as well as all 
excreta of infected birds should be burned. Abandonment of in- 
fected runs is desirable, but if this is impossible, the use of the 
Pasteur type of anthrax vaccine may be undertaken. 

Anthrax infection of soil constitutes practically a permanent con- 
dition. Opportunity for direct infection from the soil by contam- 
ination of feed, or by wounds will vary with seasonal conditions of 



228 DISEASES OF DOMESTICATED BIRDS 

moisture. Inimdations and extension of irrigation systems may 
spread the infection to new foci. On some of the infected farms 
cited by Theiler the infection seems to have first attacked cattle. In 
one case the infection had been introduced by cattle. In other out- 
breaks, ostriches died occasionally, while horses and cattle escaped. 

Every precaution should be taken to prevent the exposure of an- 
thrax-infected blood to the air. Under such conditions spores form, 
which are capable of remaining alive in the soil for an indefinite 
period. 

ASPERGILLOSIS IN ADULT OSTRICHES 

Walker has observed that in adult birds, marasmus is the only 
sign of aspergillus infection. When the lungs are affected, respira- 
tion is accelerated and the beak is kept partly open. There is pro- 
nounced loss of condition when the liver is involved. The disease 
usually runs a sub-acute or chronic course. 

The lesions are found to be more or less generalized, the liver and 
respiratory tracts being most generally involved. Degenerative 
changes in the tubercles and destructive changes in the surrounding 
tissues are marked. The tubercles may exhibit the various changes 
in the evolution of a tubercle, such as miliary granulations, caseous 
deo;eneration and fibrous transformation. The lesions in the liver 
usually consist of extensive caseous areas caused by the degenera- 
tion of agglomerated tubercles and by necrosis of adjoining liver 
tissue. 

Aspergillosis in the adult ostrich as reported by Jowett may pre- 
sent a condition very closely simulating miliary tuberculosis of the 
lungs. The lungs are consolidated, dark red in color, and are filled 
with yellowish-white miliary tubercles about the size of a pinhead, 
which stand out prominently against the background of congested 
and hepatized lung tissue. The tubercles are not readily removed 
for the perijDhery of each is united to others. They are fibrous and 
shot-like in consistency. They show no evidence of caseation nor 
calcification. There is slight thickening of the pleura, and a few 
nodules are present, but no lesions are observed in the mucosa of the 
trachea and bronchi. 

Examination for tubercle bacilli yields negative results, but mi- 
croscopic examination of crushed nodules in caustic potash reveals 
the true nature of the infection. 

Study of sectioned specimens shows that each nodule is composed 
of: (1) an unstained or very faintly stained central area, (2) sur- 



DISEASES AND PARASITES OF THE OSTRICH 229 

rounding this an intensely stained peripheral zone, and (3), sur- 
rounding all, a zone in which the air cells show inflammatory 
changes but are still pervious. The center of the nodule has under- 
gone coagulation necrosis and contains filaments and free spores. 
The next zone contains leucocytes, endothelioid or epithelioid cella 
together with many filaments. 

The fungus undoubtedly is an aspergillus, and quite likely fumi- 
gatus, although no cultures were made. 

The source of infection was regarded as moldy food. 

Archibald has reported upon aspergillosis in the Sudan ostrich, in 
which quite different lesions were observed. On opening up the res- 
piratory passage a peculiar lesion of the bronchioles is observed. The 
upper portion of a bronchus is lined by dark granular masses which 
project into its lumen. The masses are friable, but are closely ad- 
herent to the wall. The portion of a bronchiole next to the lung 
shows several " plaques " raised from the surface. These are grayish 
in color with a nodular center and vary in size from a millet seed to a 
pea. Most of them are discrete, but a few have coalesced. Their 
surface is thrown into ridges and depressions. Microscopic examina- 
tion reveals the nature of the infection. 

Aspergillosis in other birds is discussed in Chapter X. 

ASPEKGILLOSIS IN OSTRICH CHICKS 

Synonyms. Yellow liver, chick fever. 

Characterization. Aspergillosis in the ostrich chick is a highly 
fatal affection caused by aspergillus fungi^ of which Aspergillus 
fumigatus is the most common. 

History. The disease was mentioned by Douglas in 1881 who ob- 
served that it was so destructive that on some farms in Cape Prov- 
ince every chick died. 

We are indebted to Walker for making a useful experimental study 
of the various aspects of the affection, which has elucidated the 
problems of etiology and prophylaxis. 

Symptoms. In young chicks a few days old the first symptom is 
a disinclination to feed. The bird may go through the motions of 
picking, without swallowing food. The chick appears dull, weak, 
the eyes are half closed, it moves about slowly or stands, and occa- 
sionally utters a plaintive note. The neck is commonly flexed and 
the head is lowered and kept close to the body. The abdomen feels 
less tense and full than that of a healthy chick. The respiration is 



230 DISEASES OF DOMESTICATED BIRDS 

sometimes accelerated. The beak may be kept continually open, or 
only kept open during a long inspiration. The temperature is irreg- 
ular, there being a variation of 3° to 5° F. between the morning and 
evening temperatures. In healthy birds the temperature varies 
about two degrees, that is between 102° and 104° F. Sub-normal 
temperature precedes death. 

In some cases whitish nodules, about the size of a pin head may be 
detected on the buccal mucous membranes and the epiglottis. 

Destructive outbreaks of the disease occur among chicks varying 
in age from a few days to 3 or 4 weeks. It is much more prev- 
alent among artificially reared chicks than among those raised nat- 
urally. 

Death occurs within a few days after the appearance of symp- 
toms and it is seldom that an affected bird recovers. 

Morbid anatomy. In young chicks naturally infected the le- 
sions are chiefly confined to the lungs and air sacs. Less commonly 
nodules are observed on the buccal mucosa. A close examination 
of the lungs will usually reveal more or less rounded nodules aver- 
aging 1.2 mm. in diameter, and yellowish white in color. Rarely 
caseous foci or pneumonic patches are observed in the lungs. The 
lesions on the walls of the air sacs consist of either small tubercles 
or fibrinous exudate. 

The tubercles are composed of epithelioid cells, leucocytes and 
some eosinophile cells, mixed with mycelium. The duration of the 
disease in chicks is so short that caseous degeneration and fibrous 
transformation of the tubercles do not usually occur. 

Etiology. The ostrich is susceptible to several species of asper- 
gillus fungi but the one most pathogenic, and more commonly en- 
countered is Aspergillus fumigatus. A. asper also is pathogenic for 
the ostrich. The fungi are widely distributed among substances of 
importance in connection with the artificial rearing of ostriches. 
Straw may be naturally infected as also lucerne (alfalfa), and the soil 
upon which lucerne is growing. The feces of an ostrich fed upon 
lucerne are infective. 

Pathogenicity. Intravenous injection of ostrich chicks with 
spores produces a more or less generalized infection in which the 
lungs and liver particularly contain tubercles. Death occurs in from 
2 to 7 days. Inhalation of spores produces lesions in the lungs con- 
sisting of dirty white colored nodules isolated or agglomerated, and 
lesions in the air sacs consisting of nodules. Chicks varying in age 
from a few days to 31 days die in from one to ten days after the 



DISEASES AND PARASITES OF THE OSTRICH 231 

introduction of spores into the trachea. Ingestion of cultures ad- 
ministered in a gelatine capsule causes the formation of tubercles, 
but no marked intestinal changes. The oliicks die in from 5 to 18 
days. 

Dosing with the fungus in a gelatin capsule produced no effect 
upon one bird 11 days -old, and upon one adult. 

Transmission. Chicks are susceptible to infection by both in- 
halation and ingestion. Opportunity for infection exists even be- 
fore hatching, for the aspergillus fung-us often infects the air sac 
of the egg. It is capable of penetrating unbroken shell and can thus 
pass from infected to non-infected eggs. Thus chicks become in- 
fected before or during hatching, and the incubators become con- 
taminated, constituting a menace to later hatches. Infected straw 
used as bedding in chicks' sleeping boxes is a serious source of 
infection. 

Diagnosis. Aspergillosis may be identified by microscopic ex- 
amination of nodules after treatment with potassium hydrate, in 
which case the mycelium and fruiting heads may be recognized. No- 
dules planted on potato and incubated for 21 to 36 hours at 35° C. 
produce small whitish growths visible to the naked eye. After in- 
cubation for a day more the growth appears bluish in color and still 
later turns dark bluish gTcen. 

Control. Prophylaxis of aspergillosis concerns securing non-in- 
fected eggs for incubating, non-infected incubators, non-infected bed- 
ding and safe feed for the chicks. 

Treatment. No medicinal treatment is available and all efforts 
against the disease must be centered upon prevention. 

PARALYSIS OF THE OSTRICH 

Synonym. Leg-weakness. 

History. In 1900 Marx observed the disease among Sudan os- 
triches in the Frankfurt Zoological gardens. Robertson in 1900 de- 
scribed a form of paralysis occurring among ostriches near Cape 
Town. The disease is of considerable economic importance and 
seems to be becoming more common. 

Symptoms. The disease is abrupt in onset. There is sudden 
inability to rise, the interference apparently being in the toes, which 
are flexed on themselves at right angles. Tlie birds make futile and 
persistent efforts to rise, and in consequence stagger along on the hock 
joints. After a few days, effort to rise is abandoned and the paraly- 



232 DISEASES OF DOMESTICATED BIEDS 

sis eventually involves the wings and neck. Appetite remains good 
and there is no evidence of pain. Marx noted the presence of 
marked lachryniation in every case. Affected birds have been ob- 
served to live for seven months and no instance of complete recovery 
has been noted. Young birds are most commonly affected, but the 
disease may be encountered among those of any age. The disease oc- 
curs at irregular intervals in certain areas. 

Morbid anatomy. The one constant lesion as observed by Rob- 
ertson is the congestion or inflammation of the duodenum and the 
reddened appearance of the mucosa, accompanied by a deposit of 
exudate thereon. This lesion is present in some degree in all cases, 
whether early or of long standing. The sub-mucous layer of the in- 
testine is thickened and infiltrated with a clear straw colored fluid. 

Marx observed more or less peritonitis and purulent foci in the 
spleen in each case. In some cases there was enteritis with necrotic 
patches on the mucosa. 

Bacteriology. Robertson obtained from the inflamed mucosa, a 
short rod which does not stain by the Gram method. It grows fairly 
well on the common culture media under aerobic or anaerobic condi- 
tions. There is copious white growth on plain agar, glycerine agar, 
agar, gelatin and malachite green agar. On the latter the color is 
discharged along the needle track. Gas is evolved in sugar agar 
stab cultures. Growth occurs in plain bouillon, glycerine bouillon 
and sugar bouillon causing turbidity and foul odor. A brownish col- 
ored raised growth occurs on potato. Milk is not coagulated nor does 
liquefaction occur in gelatin. In natural cases, besides the organism 
in question. Staphylococcus pyogenes aureus almost invariably is pres- 
ent in cultures from the sub-mucosa of the duodenum. 

Marx isolated a non-motile, non-spore bearing. Gram negative, oval, 
bipolar staining rod, which is killed by exposure to 68° C. for an 
hour. It gTOWs readily on the ordinary culture media. Coagulation 
of milk occurs, growth on gelatin resembles that of B. coli, and a 
brownish viscid laj'or is produced on potato. Glucose is fermented 
and no indol is produced. After 24 hours on agar there appear gray- 
ish white colonies, iridescent by transmitted light which eventually 
develop into a moist greenish white layer. Bouillon becomes turbid 
in a few hours and a deposit of sediment forms in the tube. Marx 
regards the organism as belonging to the hemorrhagic septicemia 
group. 

Pathogenicity. Subcutaneous injection of 25 c.c. of a 24 hour 
culture of Robertson's organism into a cock ostrich resulted in the 



DISEASES AND PARASITES OF THE OSTEICH 233 

appearance of the typical symptoms in seven days, followed by death 
in about a month. Similar results were obtained with a number of 
other ostriches. The organism injected can be recovered from the 
lesions induced in the duodenum. Kobertson regards the symptoms 
as indicative of a poisoning. He holds the opinion that the or- 
ganisms do not invade the general tissues, but remain localized as in 
the case of diphtheria and tetanus. The poison is elaborated by the 
organism in the intestine and carried to the spinal cord and thus 
induces paralysis. 

The organism isolated by Marx was found to be pathogenic for the 
■gray mouse, pigeon, and various small birds. Guinea pigs and rab- 
bits were insusceptible. 

Control. The common source of infection is regarded as con- 
taminated food and water. Kobertson advises that infected birds be 
killed, and that the birds be shifted to bare veld and fed by hand with 
cut green crops. The continuous breeding of birds on one spot seems 
to be a factor contributing to the occurrence of the disease. 

Treatment. Gray suggests the trial of intestinal disinfection 
with cyllin, beta-naphthol, sodium salicylate, quinine or bismuth. 

WIREWOKMS IN OSTRICHES 

The wireworm, a nematode designated Trlchostrongylus douglasi, 
synonjva. Strongylus douglasi, is a parasite infesting the mucosa and 
glands of the proventriculus of the ostrich. Adult birds, if well fed 
tolerate the parasite comparatively well but ostrich chicks frequently 
succumb. This parasite occasions great losses in the ostrich farming 
industry of South Africa. 

Comparatively little was known of the life history of the wireworm 
and remedial measures until the publication of the work of Theiler 
and Robertson from which we have drawn largely in discussing the 
problem. 

Life cycle of the wireworm. The parasite undergoes four 
molts corresponding to four different stages. Two stages are en- 
countered in the life cycle outside the host and two inside the host. 
The cycle may thus be divided into a parasitic and a non-jDarasitic 
period. 

The w^ireworm in its non-parasitic stages is free living. Its fu- 
ture propae;ation and dissemination depend upon gaining access to 
the body of an ostrich. This phase of its life history is of great 
practical interest in connection with the application of measures to 
prevent the infection of clean birds. 



234 DISEASES OF DOMESTICATED BIRDS 

The egg of the wireworm is expelled from the body in the feces 
of the bird in about three days after expulsion from the worm. Ex- 
amination of feces of a number of birds has shown that one dropping 
of feces may contain from 24,000 to 600,000 eggs. A bird isolated 
under conditions preventing it from becoming reinfected has con- 
tinued to discharge worm eggs for a period of nine months without 
showing decrease in number. The limit to the time a bird will dis- 
charge eggs has not been detennined. The worm eggs in fresh drop- 
pings are non-infective. If fed to an ostrich they will be passed in 
the feces so long as they are fed, but autopsy of the bird after an 
interval will show that no worms are present. 

The worm eggs hatch only outside the body of the bird and the 
larvae undergo four molts before reaching maturity. Hatching 
and the development of the larvse are sharply controlled by tempera- 
ture and other conditions. At a temperature of 98° F. ova hatch and 
the larvse reach maturity. At 100° to 101° F. hatching occurs, but 
only the older larvse reach maturity. The same is true of a tempera- 
ture range of 102-102.5° F. A temperature of 104° F. does not 
permit the development of larvse. Ova and larvse in the first stage 
may be kept dry at room temperature for two years and develop to 
maturity when moistened. Ova and first stage larvse cease develop- 
ment when dried over calcium chloride, but remain alive for at least 
three years. Eggs retain their vitality in water but cannot reach ma- 
turity at a depth of two or three inches. The vitality of eggs is not 
destroyed by a temperature of 32° to 46° F. for three months. 
Droppings kept under natural outdoor conditions for fifteen months 
contain live mature larvse and first stage larvse. 

Larvse in the first stage and immature larvse of the second stage 
do not develop in the stomach of the ostrich. Mature second stage 
larvse alone are capable of becoming established there. Liquid is 
imdoubtedly a suitable medium for these larvse and they are very 
active in such an environment. A temperature below 38° F. checks 
their movement under these conditions. When droppings and sec- 
ond stage (mature) larvse are left exposed on soil where grass 
is growing, the larvse crawl to the tip of the grass blades where they 
are more numerous than on the portion below. They have been ob- 
served to remain alive on gTeen grass for six months and for two 
months more after the grass dried up although in diminished num- 
ber. On a second crop of grass, larvse were observed at a height 
never exceeding three inches. From one infection of the soil larvse 
were found on grass up to 14 months and at 17 months in the drop- 



DISEASES AND PARASITES OF THE OSTEICH 235 

pings originally placed on the soil. The propensity of larvae for 
climbing vegetation results in rendering infective, any ostrich fodder 
raised on land contaminated by the droppings of infected birds. 
Mature larvae will remain alive in a moist atmosphere at room tem- 
perature for fifteen months. They will remain alive in water at a 
low temperature for 13 months. After being kept in ice at a tem- 
perature of 16° to 28° F. for 11 days and released by melting the 
ice, they revive. Larvge will travel through soil, so no benefit can 
i-esult from plowing infected ground. 

The possibility that mature larvse pass through the skin of the 
ostrich to reach the stomach has been tested by experiment, with neg- 
ative conclusions. Sheep and fowls do not serve as hosts for the 
wireworm. 

Mature larva? outside the ostrich may be killed by a liberal ap- 
plication of carbolic acid or lysol in 5 or 6 per cent solution. Sul- 
phuric and hydrochloric acids are effective. 

On gaining access to the ostrich, the larvae pass through the third 
and fourth larval stages and develop into the adult worm after the 
fourth molt. 

Ostrich chicks may succumb to infestation by these lan^ae in the 
parasitic stages, before they develop into adult worms. 

Adult birds can tolerate an excessive infestation with wireworm 
provided they are well fed. Once infested, an ostrich will remain 
infective for years and constitute a source of contamination of the 
soil. An infected pasture or pen will remain infected for years by 
reason of the presence of eggs and larvae. 

Morbid anatomy. The wireworms are found in the proventric- 
ulus in the lumina of certain deep glands or lying between superficial 
tubular glands or in the depths of the mucosa of certain areas of the 
organ near the entrance of the esophagus. They are demonstrated 
in the fresh stomach by scraping off the mucous layer of the mucosa. 
They are very rarely on the surface but proceed thence upon reach- 
ing maturity. The effect of infestation becomes evident after about 
the Sith day after infection, and subsequently. The layer of mucus 
becomes detached in parts and hemorrhagic infiltration of the mu- 
cosa appears. When the worms are numerous and mature, the mu- 
cosa appears swollen and is covered by a copious amount of mucus. 
This condition designated " vrotmag " (rotten stomach) by the Boers, 
causes anemia and emaciation of the birds. 

Diagnosis. The presence of worms may be determined by worm 
cultures, that is by placing fresh droppings in a wineglass which is 



236 DISEASES OE DOMESTICATED BIKDS 

covered to prevent evaporation. If the bird is infected, larvae recog- 
nizable with the naked eye, will after a time be seen on the glass. 
The number present furnishes a rough indication of the extent of the 
infection. 

Prevention. It is possible to raise ostrich chicks free from in- 
fection when suitable precautions are carried out. Small runs 50 by 
150 feet are quite large enough. If clean gTound over which os- 
triches have not run is not available, it is possible to render an area 
safe by removing the soil to a depth of three inches. The runs should 
be so located that there is no contact with infected birds, and so that 
there is no possibility of infection through drainage into them. The 
runs should be stocked with incubator chicks, or chicks removed from 
the nest immediately after hatching. The feed will be of the usual 
character, derived from land that has not been contaminated by in- 
fected birds. If hens are kept with the chicks, all feces of the adult 
birds should be picked up daily. These jDrecautions will permit 
raising ostrich chicks to such an age that wireworm infestation is 
no longer dangerous to the birds, and has the additional advantage 
of preventing sclerostome and tapeworm infestation. 

Treatment. JSTo treatment has been discovered which can be de- 
pended upon to expel all the worms from an infected bird. The lo- 
cation of the worms in the mucosa and glands is such as to dis- 
courage belief that a successful treatment will be found. A num- 
ber of substances when tested in vitro are undoubtedly effective in 
killing the parasites. A number of methods of treatment have 
been tested by Theiler and Robertson, who judged the effect by ob- 
serving the influence of the treatment on the numbers of eggs in the 
feces both by microscopical observation and by worm cultures. 

Carbolic acid in a dose of 300 c.c. of a 2.5 per cent solution caused 
the eggs to become rare for 14 days after which they became as 
numerous as they were before treatment. Several trials with this 
agent led to the conclusion that the dose employed, which is equiva- 
lent to 7.5 grams of pure carbolic acid, checks the laying of eggs for 
a while without killing all the worms. 

A treatment was tried which consists of administering 300 c.c. of 
paraffin (kerosene) , followed after 24 hours by 1 ounce each of slaked 
lime and of sal-ammoniac. It has been claimed that the paraffin dis- 
solves the mucus-like layer over the worm infested area, and that the 
ammonia resulting from the reaction between the drugs administered 
later kills the worms. However, the trial failed to demonstrate any 
effect upon the worms. 



DISEASES AND PAKASITES OF THE OSTRICH 237 

Dosing with thymol in quantities as large as 12 grams had only 
a temporary effect in checking the laying of eggs for a few days. 

Beta-naphthol in repeated enormous doses and followed after sev- 
eral days with 250 grams of magnesium sulphate merely checked the 
laying of eggs for a few days. 

Santonin in 10 gram doses produced some influence on the num- 
ber of eggs present after treatment. 

Kamala in doses of 20 and of 40 grams produced no apparent ef- 
fect. Flores koso in doses of 50 and of 100 grams merely produced 
some influence on the number of eggs. 

Liquid ammonia proved inefl^ective and even harmful to birds re- 
ceiving the treatment. Carbon bisulphide in a dose of 30 c.c. in 
lYO c.c. of olive oil or in a dose of 20 c.c. in a gelatin capsule, proved 
ineffective. 

Apart from the fact that the worms are well protected in their 
location in the mucosa, certain anatomical considerations prevent 
drugs from acting unless the fluid fills the whole stomach and raises 
the fluid to the level necessary to bring it in contact with the areas 
infested with worms. This is almost impossible to accomplish since 
the intestinal opening is so low as to drain out fluid. 

TAPEWORM OF THE OSTRICH 

The tapeworm of the ostrich is known as Tcunia struthionis, and 
is chiefly a parasite of the young. Chicks may become infested 
when only three weeks old and from that age until two years, tape- 
worms constitute a very common parasite. The worms reach two 
or three feet in length and may almost plug the intestine. Robert- 
son reports having observed in one ostrich nine months old, over two 
hundred tapeworms with a weight of nearly three . pounds. The 
aggregate harm done by these in abstracting nutriment and in in- 
juring the mucosa at the point of attachment, must have been con- 
siderable. On the other hand, the occurrence of tapeworms in the 
adult ostrich, is rarely observed. The intermediate host of the os- 
trich tapeworm is not known. 

Symptoms. Under good conditions an ostrich may tolerate a 
heavy infestation without showing symptoms. If food becomes 
scarce, climate becomes unfavorable, or the chick becomes ill from 
some cause, the bird exhibits evidence of the presence of the worms. 
There is general ill health, and the mucosae of eyes and mouth are 
pale. The presence of ripe segments of tapewonn in the droppings is 



% 



238 DISEASES OF DOMESTICATED BIRDS 

the one certain symptom. The segments are always found on the out- 
side of the dung pellets. 

Treatment. Robertson recommends the use of petrol or motor 
car spirit, Pratt's green label (gasoline). It is advisable to fast the 
chicks a little before dosing, but if weak and thin, they should not 
be starved before the first dose. The dosage for various ages as 
recommended by Robertson, is 

1 and 2 months old birds receive I/2 oz. 

3 months old birds receive 1 oz. 

4 months old birds receive 2 oz. 

5 months old birds receive 3 oz. 

6 months old birds receive 4 oz. 

7 to 11 months old birds receive 5 oz. 
12 months old birds receive 6 oz. 
Full grown birds receive 8 oz. 

The petrol is given pure and not mixed with water. It volatilizes 
at a temperature below that of the body of the bird, and consequently 
permeates the whole intestinal tract in a short time. 

Care must be taken in drenching, for even a little fluid gaining 
access to the trachea may be followed by serious or even fatal con- 
sequences. In drenching birds, the entrance to the windpipe should 
be covered with the fingers of one hand while the bottle of petrol is 
passed over them. The head of the bird should be held up for a 
few minutes after drenching to prevent the possibility of regurgi- 
tation. 

Hutcheon has employed liquid extract of male fern in a dose 
varying from a teaspoonful for a young ostrich three or four months 
old, to a tablespoonful for a full gi'own bird. He has also used 
turpentine in a dose varying from a dessertspoonful to two table- 
spoonfuls. It is more effective when combined with a purgative such 
as linseed or castor oil. 



FILARIA OF THE OSTRICH 

A gigantic nematode of the ostrich, designated Filaria spicularia 
occurs in the subperitoneal connective tissue and also in the sub- 
lumbar region. The parasites vary in length from a quarter of a 
meter to a meter and are coiled together in such a complex manner 
that it is difiicult to secure a whole specimen. The presence of 
the parasite appears to have no effect upon the health of the birds. 



DISEASES AND PARASITES OF THE OSTRICH 239 



LEUCOCYTOZOON INFECTION IN OSTRICH CHICKS 

Walker has observed a leiicocytozoon infection in ostrich chicks 
varying; in age from 4 weeks to 7 months. 

Symptoms. There is a disinclination to feed, loss of condition, 
stunted growtli and paleness of the buccal mucous membrane. The 
skin of the body and around the eye is bluish colored. When the 
chicks are driven, the affected ones are unable to keep up with the 
rest of the flock. Sickness is noted several days before death. 

Morbid anatomy. Microscopic examination of the organs shows 
no constant lesions. Examination of the blood frequently reveals the 
presence of a leucocytozoon. The observations lead Walker to the 
conclusion that it will be necessary to ascertain whether the leucocy- 
tozoon enters into the etiology of diseases of ostrich chicks. 

Etiology. The organism is designated Leucocytozoon struthionis. 
It occurs in young chicks but has not been found in adult ostriches. 
In dried blood smears fixed with methyl alcohol and stained with Gi- 
emsa, two main types of parasites are observed which apparently cor- 
respond to male and female gametocytes. 

The female gametocyte occurs most frequently. The shape is more 
or less rounded but may be irregular, due to distortion brought about 
in preparing the smears. The organism varies from 11 to 15 microns 
in length and from 9 to 13 microns in width. The protoplasm stains 
deeper than does that of the male gametocyte and scattered through 
the protoplasm are a number of metachromatic granules. These ap- 
pear more distinctly in some of the parasites than in others. A num- 
ber of small clear spaces occur throughout the protoplasm. The nu- 
cleus is represented by an aggregation of small chromatin granules 
generally at the center or near the edge. In most instances a large 
chromatin granule stands out distinctly. It is situated in the mass of 
granules, or at the side of them, or at some distance from them. The 
nucleus of the host cell is always altered in shape. In most cases it is 
elongated and located at the margin of the parasite. 

The male gametocyte is usually more or less rounded and is smaller 
than the female. The protoplasm stains less densely than that of the 
female. The chromatin granules of the nucleus are generally scat- 
tered throughout the cell. Sometimes they are larger and widely sep- 
arated and are observed very distinctly. The nucleus of the host cell 
is irregular in shape and is found at the edge of the parasite. It is 
less elongated and smaller than in the case of the cell invaded by the 
female. 



240 DISEASES OF DOMESTICATED BIKDS 

'No spindle shaped formation of the host cell has been observed in 
emears from ostriches. 

ACOEN POISONING IN THE OSTRICH 

Robertson has observed a number of cases in which acorns have 
killed ostriches. These when consumed in moderation constitute a 
safe and excellent feed. However, when birds have access to a boun- 
tiful supply, they will gorge themselves with fatal result. The in- 
jury is caused by the astringent action of the tannic acid. 

Symptoms. The birds lie down persistently, seem constipated, 
strain and appear giddy. They stagger on tiptoe balancing them- 
selves with their wings. The feces consist of nearly cylindrical pel- 
lets of very hard material. The urine closely resembles green paint. 
Some birds twist their necks as if in pain. 

Morbid anatomy. Lungs, heart, liver and spleen appear normal. 
The stomach contains undigested acorns. The intestines show evi- 
dence of constipation with subsequent congestion. The duodenum is 
swollen, thickened and congested with blood. The mucosa shows 
acute inflammation and is covered with a dirty, grayish white deposit 
or slime. On scraping this off the mucosa is seen to be very red. 
The colon is packed with pellets of hard dung which are black in 
color and covered with a gray slime with traces of blood. The mucosa 
of the colon is also highly reddened. The ceca are packed with 
masses of hard dung. 

Treatment. The afi^ected bird is given 25 ounces of raw linseed 
oil to which is added 4 drams of powdered Barbadoes aloes which 
previously has been dissolved in a little warm water. Twelve hours 
later each bird is given one ounce of bicarbonate of soda dissolved 
in water. Birds that refuse to eat may be drenched with gruel, raw 
eggs and brandy several times a day. 

REFERENCES 

1. Archibald. Aspergillosis in the Sudan ostrich. J. Comp. Path, and 
Therap., Vol. 26, 1913, p. lYl. 

2. Jowett. Pulmonary mycosis in the ostrich. J. Comp, Path, and 
Therap., Vol. 26, 1913, p. 253. 

3. Marx. Ueber ein Infectiose Krankheit der Strausse. Centralhl. f. 
BaUeriol. {Etc.), 1 Alt. Orig., Bd. 27, 1900, S. 822. 

4. Neumann. La filaire de I'autruclie (Filaria spicularia). Rev. Vet., 
T. 66, 1909, p. 544. 

5. Robertson. Paralysis in the ostrich. J. Comp. Path, and Ther., 
Vol. 23, 1910, p. 182. 



DISEASES AND PARASITES OF THE OSTRICH 241 

6. Robertson. Notes on ostrich parasites. Agr. J. Cape of Good 
Hope, Vol. 33, 1908, p. 583. 

7. Theiler. Anthrax in the ostrich. Agr. J. Union of So. Africa, Vol. 
4, 1912, p. 370. 

8. Theiler and Robertson. Investigations into the life history of the 
wire-worm in ostriches. Union of So. Africa, Dep. Agr., Ann. Kpts. Dir. 
Vet. Res., 3^, 1915, p. 215. 

9. Walker. Aspergillosis in the ostrich chick. Union of So. Africa, 
Dep. Agr., Ann. Rpts. Dir. Vet. Res., 3-4, 1915, p. 535. 



CHAPTER XIX 

INFECTIOUS DISEASES OF GEESE AND DUCKS 
GOOSE SEPTICEMIA 

History. Curtice in cooperation with Smith described several 
outbreaks of hemorrhagic septicemia among geese in Rhode Island. 
The disease occurred in one establishment among geese kept in lots 
of 300 each in fattening pens. The birds were assembled from 
various farms in numerous small lots, any one of which might have 
contained infected birds. Subsequent handling of the birds in the 
fattening pens involved separating them according to condition, which 
practice brought about extensive intermingling of birds. 

Etiology. The etiological agent is a member of the hemorrhagic 
septicemia gToup which has become well adapted to waterfowl, geese 
in particular. 

Pathogenicity. Geese are susceptible to infection by feeding cul- 
tures while ducks and hens are not. Geese, ducks, rabbits, mice and 
pigeons are susceptible to subcutaneous injection and hens are not. 
After exposure by feeding or by subcutaneous inoculation, death oc- 
curs in less than thirty-six hours. Feeding culture to a goose may 
cause death in less than seventeen hours. 

Symptoms. It is characteristic of the disease that birds are 
found dead at feeding time, mornings or evenings, without having 
shown sickness. Symptoms occasionally are observed during the 
last hour or so before death and largely concern the death struggles. 
The gait becomes uncertain, the head is burrowed in the dirt and 
is twisted. 

Morbid anatomy. There is considerable mucus in the throat 
and mouth, and very tenacious mucus in the nasal cavity. The veins 
of the head seem congested as if the bird had died of asphyxia. The 
mucosa of the intestine is studded with ecchymoses or larger hem- 
orrhagic areas. In about half of the cases, the liver is studded with 
necrotic foci. Epicarditis and pericarditis are present occasionally 
as also is involvement of the lung. 

Treatment. Medicinal treatment is unavailing. 

Prophylaxis. Preventive measures will include precautions 

242 



INFECTIOUS DISEASES OF GEESE AND DUCKS 243 

such as restricting the number of birds in contact with one another 
and other similar precautions aimed at restricting the spread of in- 
fection. 

EXUDATIVE SEPTICEMIA OF GEESE 

Synonyms. Ansteckende Luftsackentziindung der Giinse, Ganse- 
Influenza. 

Characterization. Exudative septicemia is an infectious septi- 
cemic disease of geese distinguished by the formation of fibrinous 
exudate upon the pericardium, liver and intestines and caused by 
Bacillus ansenim exudativa'. 

History. The disease has been observed by Frosch and Birn- 
baiun, Loffler and also by Riemer. Bugge studied a similar disease 
and while he does not give details concerning the organism present, it 
is possible that he encountered the same infection. 

Geographic distribution. The disease seems to have been recog- 
nized unquestionably only in Germany. The occurrence of the dis- 
ease among geese imported into Germany from Russia would indicate 
that it exists in the latter country also. M'Fadyean has described a 
septicemia observed in geese in England which resembles the disease 
in question in several particulars. 

Symptoms. The existence of the disease is first indicated by loss 
of appetite. The breathing may be accelerated, with the beak open 
and accompanied by a snoring sound. Coughing and choking may 
occur. The bird separates from the flock, squats frequently and rises 
with difiiculty. Diarrhea occurs within 24 hours of death. The 
bird becomes progressively weaker and dies in from two to five days. 

Morbid anatomy. The most striking lesion is the presence of a 
fibrinous exudate upon various structures in the body cavity. The 
surface of the liver is covered by a thin, fibrinous, yellowish white 
layer which is easily detached. The exudate may extend between 
loops of the intestines, the air sacs, the pericardium and the e])i- 
cardium. Fluid exudate may also be present. The pericardial sac 
contains serous, cloudy fluid. The bronchi in some cases are 
plugged with yellowish, fibrinous, purulent material. The liver 
is usually slightly enlarged and may contain small spots. The 
spleen and kidneys are also enlarged. The mucous membrane of 
the intestine is swollen, reddened and contains small hemorrhages. 

Etiology. The infection is caused by Bacillus septicemia an- 
serum exudativce described by Riemer. This is a small slim rod 
varying in length from .5 to 1.5 microns and .5 to 1. micron broad. 



244 DISEASES OF DOMESTICATED BIRDS 

The cells frequently lie in pairs, so that they appear like diplococci. 
The organism is always found in great numbers in the heart blood, 
the pericardial fluid and in the fibrinous exudate. It is stained 
readily by the common anilin dyes, and best by carbol fuchsin. The 
organism is Gram negative, non-motile and does not form spores. 
Indol production is not observed except perhaps in traces in old 
cultures. 

Frosch and Birnbaum succeeded in growing the organism at first 
only on medium containing hemoglobin. The first generation out 
of the goose grew on plain agar and bouillon when plenty of blood 
was carried over to the medium in making the inoculation. Pigeon 
blood agar induced growth but after many transfers failed. A 
medium rich in hemoglobin made as follows was more successful. 
Defibrinated horse blood is mixed with equal parts of distilled 
water to cause the liberation of the hemoglobin. About 1 c.c. of 
this solution is added to each tube of melted, cooled agar. The 
agar is then shaken and is subjected to fractional sterilization at 
Y0° C. for three days. On hemoglobin agar so prepared, the organ- 
isms form a luxuriant gTayish white growth. In smears from such 
cultures the rods appear somewhat larger than in smears from the 
animal body and very frequently long thread-like forms are ob- 
served. 

On common agar of slightly alkaline reaction it forms in 24 to 
36 hours a luxuriant grayish white, transparent, slightly opalescent 
layer, which in older cultures becomes brownish yellow in color. 
The condensation water contains considerable sediment. The 
optimum growth temperature is 37° to 38° C. No growth occurs on 
acid agar. 

The period of life of a culture is limited. By holding at room 
temperature, transfers succeeded at 14 days, but many transfers 
fail sooner. The cultures in the incubator nearly all die within 8 
days. 

A slight uniform clouding occurs in bouillon, which after some 
days contains a limited amount of sediment which on twisting, forms 
a spiral column. In some cultures a pellicle is formed of thread- 
like grov^h. 

In gelatin stab cultures held at 21° C, a slight non-characteristic 
growth is observed in the vicinity of the line of inoculation, and on 
the surface. After some time a funnel-shaped area of liquefaction 
forms slowly, and complete liquefaction eventually occurs. Growth 
on gelatin plates is accompanied by liquefaction and offers no char- 
acteristic features. 



INFECTIOUS DISEASES OF GEESE AND DUCKS 245 

Glucose and lactose bouillon are uniformly clouded but gas forma- 
tion does not occur. In lactose there is no change in reaction, but 
in glucose there is a slight reduction of alkalinity. 

A luxuriant growth occurs in the form of a whitish yellow layer 
on Loffler's serum. On potato a thin shin^^, yellowish white layer is 
observed at 24 to 48 hours, which later becomes brownish in color. 
Growth does not occur on Drigalski-Conradi nor Endo plates. Milk 
is not coagulated. Riemer and Loffler both regard the organism as 
belonging to the influenza group. 

Pathogenicity. The organism is markedly pathogenic for 
geese, which are infected most certainly by intramuscular injection. 
The musculature in the vicinity of the point of inoculation is colored 
grayish white over a large area. An attempt by Frosch and Bii*n- 
baum to infect a grown goose by feeding with organs of a goose dead 
of the disease, failed, as did a similar experiment by Riemer in 
which bouillon culture was used. In neither case were goslings 
available. 

The latter author observed that either intramuscular or subcu- 
taneous injection caused sickness followed by death in from 36 to 
Y2 hours. In artificially infected birds the fibrinous exudate on 
the liver may not be found, due to the unnatural rapidity of the 
course of the disease. 

Rabbits, gray and mixed rats, mice, white mice, hens, and pigeons 
are refractory to inoculation. Guinea pigs have succumbed to an 
intraperitoneal inoculation of a suspension of the growth from one 
agar culture. They withstand smaller amounts, such as 1 to 3 
loops. 

Riemer succeeded in infecting an 8 weeks old duck by intra- 
muscular injection of a suspension from an agar culture. Of three 
grown ducks, only one became infected by intramuscular injection. 

M'Fadyean in England examined a few geese dead from a septi- 
cemic infection. Smears from the blood contained great numbers 
of organisms which were cylindrical rather than ovoid in outline. 
Beyond a slight inflammation of the intestine, no lesions w^ere ob- 
served. Agar tubes seeded from the heart blood failed to show 
growth, and cultures kept under anaerobic conditions likewise failed. 
The organism was Gram negative, and was not pathogenic to the 
mouse, the rabbit, the hen, the guinea pig, the pigeon or to one duck. 
Transmission to a goose by feeding failed, but succeeded when sub- 
cutaneous inoculation was employed. The writer concluded that 
the disease was not fowl cholera. ISTone of the observations made 
deny the possibility that the infection was exudative septicemia. 



N 



246 DISEASES OF DOMESTICATED BIKDS 

Prevention. Individual isolation of birds is the most effective 
means of preventing the spread of the infection. General disinfec- 
tion is indicated. 



OSTEO AETHKITIS IN YOUNG GEESE AND DUCKS 

Synonyms. Osteo arthrite aigue des jeunes oies, French; osteo- 
arthritis bei jungen Giinsen und Enten, German. 

Characterization. The affection consists principally of a serous 
or sero-fibrinous arthritis, hemorrhagic inflammation of the bone 
marrow and intestinal catarrh. 

Geographical distribution. Outbreaks have been reported in 
France, Germany and in the latter country among birds that had 
recently been imported from Russia. It is reported as generally 
distributed in Germany. 

History. The disease was first described by Lucet in France in 
1892, by Freese in Germany in 1903, and by Hasenkamp and 
Sachweh in the same country in 1914. 

Etiology. Pus from all joints examined bacteriologically yields 
pure cultures of Staphylococcus pyogenes aureus which, however, 
forms but little pigment. The organism is recognized microscopi- 
cally in pus in gTeat numbers and a few are observed in smears from 
heart blood. 

Pathogenicity. Only young geese and ducks are susceptible, of 
which 90 per cent become affected. Old geese and ducks, hens and 
pigeons are immune. Hasenkamp and Sachweh report one instance 
of finding a dead hen in an establishment where ducks were infected, 
but made no bacteriological examination. 

The hen, pigeon and rabbit injected subcutaneously with blood 
of an infected bird, remain healthy. The hen and pigeon likewise 
are not affected by subcutaneous injection of pus from the joint of 
an affected bird. Hasenkamp and Sachweh have infected hens and 
pigeons by intravenous inoculation. 

The disease is transmitted to young ducks by intravenous inocula- 
tion with culture of S. pyogenes aureus. Subcutaneous inoculation 
or ingestion have failed to induce infection. 

Mortality. Loffler observed an outbreak of the disease among 
346 geese, of which 43 were old, and 313 young ones. Of the 346 
geese, 191 became sick. Of these latter 5 were old and 186 were 
young. One old one and 159 young died. The mortality among 
the young ones was 85.5 while that of the old ones was 20 per cent. 



INFECTIOUS DISEASES OF GEESE AND DUCKS 247 

Symptoms. In general the disease is manifested in two forms, 
either as a pure acute type with rapidly fatal result, or as a chronic 
form terminating in death or recovery after a long time. 

In the acute type as described by Freese, young geese and ducks 
appear apathetic and eat less. When driven it is seen that they are 
very lame in one or the other leg. The joints of the legs are swollen, 
fluctuating, hot and very painful. Usually only a few joints are in- 
volved, among them most frequently the hock and single toe joints. 
The wing joints may also be involved and of these frequently the 
elbow is involved. In this case, the affected wing droops. Besides 
s^anptoms of arthritis one observes severe diarrhea and often a 
slight mucous catarrh of the conjunctivae. Birds showing the acute 
symptoms die in from two to four days. 

In the chronic form of the disease the arthritis is the most promi- 
nent feature of the clinical picture while the general symptoms are 
less marked. There is a slight diarrhea during the first few days 
and apj)etite does not entirely disappear. The birds do not appear 
quite apathetic but frequently make efforts to walk. They become 
greatly emaciated. These symptoms may last for various lengths 
of time, on the average, 14 days. Then, either death occurs or the 
birds improve with gradual disappearance of symptoms of acute 
arthritis. Nevertheless in many cases a painless swelling of cer- 
tain joints remains for weeks. In this case the birds walk stiffly for 
a long time. They remain halted in development so that they are 
not suitable for fattening. In isolated cases during the chronic 
course, an acute relapse may occur followed by death. 

Lucet describes two types of the disease. One, designated as the 
peracute type, is rapidly fatal. In this, the osseous lesions are 
slightly pronounced or sometimes inappreciable. The other type, 
the acute, is accompanied by epiphyseal osteitis and arthritis. The 
duration of the disease is much longer and is terminated by death 
after a variable time or by recovery. 

In the acute type as observed by Lucet there is depression, the 
head is bowed, the feathers are ruffled, dirty and dull. The mucosae 
are pale, diarrhea occurs, there is no appetite and the rectal tempera- 
ture is markedly elevated. The infected subjects lag behind the 
others, walk with difficulty, limp and assume a crouching position 
frequently. All these symptoms rapidly become aggravated. The 
upright position becomes impossible, the members are incapable of 
movement and the collapse is extreme. The head rests on the 
ground by the beak. Death occurs in one, two or three hours. 



248 DISEASES OF DOMESTICATED BIEDS 

The acute form is much more common and because of its slower 
development is much better defined. First there is depression, 
rutfling of the feathers, diarrhea, elevation of the rectal temperature 
and loss of appetite all of which are common to serious diseases. 
This period of development more or less accentuated has a somewhat 
irregular duration. Sometimes it precedes the local symptoms by 
several days, at other times it is hardly appreciable. Walking be- 
comes difficult and painful. There is lameness in one or both legs. 
The j)atient lags behind its fellows, sits on the ground and assumes 
the upright position with difficulty. At this stage the important 
joints, especially the tibio metatarsal joints, singly or together are 
the site of precise pathological manifestations. They are enlarged, 
doughy, very painful and execute very limited movements. Some- 
times they are completely immobilized. The temj^erature reaches 
36° to 38° C. when under normal conditions it would be 30° or 
34° C. 

Incapable of moving, the geese remain in the sternal position for 
entire days with the feet underneath them or extended behind or even 
sideways. The wings droop, the bird is depressed, holds the beak 
down and eats with pain. Sometimes one which is less ill attempts 
to flee when approached. With neck stretched out, with beak 
opened, and whistling it flaps the wings and drags itself along for 
several steps before stopping exhausted. 

In such a condition, two terminations are possible. There may 
be increase of depression, diarrhea and pallor of the mucous mem- 
branes. The cutaneous parasites become more numerous, the 
emaciation and cachexia increase and death follows after one, two 
or three weeks. On the other hand, the general symptoms diminish 
in intensity, the appetite returns, the movements become easier and 
recovery occurs after a variable time. 

Complete recovery is rare. The affected joints never return to 
their normal size nor their former mobility. Ankyloses, thick- 
enings and irregularities of the joints interfere with movement. 

Morbid anatomy. The carcass is greatly emaciated. The 
mucosa of the beginning and end portions of the intestine is greatly 
swollen and diffusely reddened or slate gray in color. The abundant 
contents of the intestines are viscid and possess a reddish gray color. 
The intestinal inflammation is most marked in the pure acute type 
in which case, dark red petechise occur in the mucosa. The spleen 
is hypertrophied and the liver is always enlarged. 

The affected joints are more or less swollen and filled with either 



INFECTIOUS DISEASES OF GEESE AND DUCKS 249 

a pure serous fluid or a sero-fibrinous exudate. The fibrin occurs 
mostly as a yellowish, transparent layer on the joint cartilages and 
on the inner wall of the joint capsule. 

The exudate is present in various amounts. The synovial mem- 
brane of the joint capsule is swollen and reddened in the acute cases. 

The bone marrow is very shiny, dark red in color and the consist- 
ency is strikingly soft, often fluid. 

In the chronic form the joint cartilage is involved in spots and is 
easily lifted from the tissues beneath. Under these spots, the bone 
has a porous, rough consistency. In the epiphyses of the bone are 
noted cavities of various sizes which are filled with dry, crumbly, 
grayish yellow masses. These when rubbed between the fingers feel 
granular and are regarded as bone pus. Freese observes that pus 
in birds has this consistency instead of the creamy-like character 
of that occurring in mammals. In other epiphyses there are holes 
in the joint cartilage which communicate directly from the joint to 
the cavities in the bone described above. In such cases the joints 
contain more or less of the bone pus. The bone of the altered epi- 
physes is covered on the outer surface with a cartilage-like deposit, 
which is easily overlooked. 

Prevention. Prophylactic measures should include separation 
of the sound birds from infected ones, disinfection of the quarters, 
proper disposal of the dead and of the manure. 

Treatment. The advisability of local treatment with counter 
irritants and disinfection might be considered. 



SEPTICEMIA OF DUCKS 

Lisi has described a fatal septicemia of ducks in which all birds 
exposed to the infection succumbed. 

Etiology. The causative organism is present in the various 
exudates, organs and in small numbers in the blood. It is somewhat 
larger than that of fowl cholera. The organism grows on gelatin, 
causing slow liquefaction and forms a brown colored layer on potato. 

Pathogenicity. Inoculation of ducks with culture causes death 
in ten or twelve hours. Rabbits and guinea pigs succumb in three 
days. The fowl is refractory. The white rat is somewhat suscept- 
ible and an area of caseous infiltration forms at the point of inocula- 
tion. 

Symptoms. The advent of symptoms is abrupt, the eyes are 
closed and lachrymating. The bird appears depressed and remains 



250 DISEASES OF DOMESTICATED BIRDS 

in one position a long time without moving. Death occurs in from 
one to four hours. 

Morbid anatomy. The eyelids are closed with a purulent secre- 
tion, the cornea is covered with white spots, the aqueous humor some- 
times is opaque. The pericardium contains a gelatinous exudate 
and the heart muscle is pale. The liver is softened, the intestines 
and mesentery are congested. A fibrinous exudate occurs on the 
peritoneum of some birds. 

DUCK CHOLERA 

Comil and Toupet described a disease of ducks which resembles 
fowl cholera very closely. The authors differentiate it from that 
disease on the basis of the non-susceptibility of fowls and pigeons 
to cultures of the organism isolated from the ducks. 

SEPTICEMIC INFECTION OF WATERFOWL 

Willach observed a cholera-like infection among waterfowl. The 
outbreak involved Pekin ducks, swans and geese. 

Symptoms. The affected birds show dullness, apathy, inap- 
petence, marked thirst, difficulty in swallowing and hoarseness. 
They die suddenly without spasms. 

Morbid anatomy. Autopsy reveals lesions of fowl cholera. 

Etiology. Examination of the blood reveals an organism resem- 
bling that of fowl cholera. However, it differs from it in several 
particulars. 

Pathogenicity. Hens, ducks, pigeons and mice succumb to the 
infection. 

REFERENCES 

1. Bugge. Ansteckende Luftsackentziindung der Ganse. Zeltschr. f. 
InfelcHonsl-r. d. Haustiere, Bd. 3, 1907, p. 470. 

2. Curtice. Goose septicemia. Ehode Island Agr. Exp. Sta. Bull. 86, 
1902. 

3. Cornil et Toupet. Sur eine nouvelle maladie bactenenne du canard 
(cholera des canards). Com,pt. rend. Soc. de liol., T. 106, 1888, p. 1747. 

4. Ereese. ITeber eine durch den Staphylococcus pyogenes aureus 
hervorgerufene Osteo-Arthritis bei jungen Gansen und Enten. Deutsche 
tierdrztl. Wchnschr., Bd. 15, 1907, S. 322. 

5. Erosch u. Birnbaum. Ueber eine durch den Bacillus septicsemife 
anserum exudativa; (Kiemer) bedingte Ganseseuche, Zugleich ein Beitrag 
zur Erage dere Pseudoinfluenzabacillen, Centralhl f. BaUeriol. {Etc.). 
1 Alt. Orig., Bd. 52, 1909, S. 433. 



INFECTIOUS DISEASES OE GEESE AND DUCKS 251 

6. Hasenkamp unci Sachweh. Staphylokokken-Erkrankungen beim 
Geflugel. Ticrdrztliche Rundschau, Bd. 20, 1914, S. 85. 

7. Loffler. Ueber eine in Jahre 1904 in Klein-Kiesow bei Greifsweld 
beobachtete Ganseseuche. Arch. f. Tierheilk., Suppl. Bd. 36, 1910, S. 289. 

8. Lisi. Infezzione setticoemia in una branco di anatrini. II moderno 
zooiatio, 1896, p. 415. 

9. Lucet. De I'osteo-arthrite aigue infectieuse des jeunes oies. Ann. 
de V Inst. Pasteur, T. 6, 1892, p. 841. 

10. M'Fadyean. A remarkable outbreak of goose septicemia. /. Comp. 
Path, and fherap.. Vol. 15, 1902, p. 162. 

11. Riemer. Kurze Mitteilung iiber eine bei Gansen beobachtete ex- 
sudative Septikamie und deren Errger. Centralhl. f. Bakteriol. {Etc.), 
1 AU. Orig., Bd. 37, 1905, S. 641. 

12. Willach. Eine Cholera unter dem Wassergefliigel in Schwetzingen. 
Deutsche tierdrztl. Wchnschr., 1895, No. 51. Abstracted in Centralhl. 
f. BaUenol. {Etc.), 1 AU. Orig., Bd. 20, 1896, S. 187. 



CHAPTER XX 

INFECTIOUS DISEASES OF CANARY BIRDS 

Infectious diseases of canary birds cause heavy losses in breeding 
establishmen.s where hundreds of birds are kept in close contact 
with one another. These conditions, and the occasional introduction 
of breeding stock furnish favorable circumstances for the spread of 
disease, and severe losses occur. The literature contains references 
to a number of infections chiefly observed in Germany where canary 
breeding attains considerable importance. Careful comparison of 
the descriptions of canary bird infections indicates that most of those 
described fall into one of two groups. One, designated infectious 
necrosis is caused by a member of the hemorrhagic septicemia group, 
and another is caused by B. jmratyphosus B. 

INFECTIOUS NECROSIS OF CANARIES 

Synonyms. Bird fever, canary fever, septic fever and bird 
plague. 

Characterization. The disease is an infection chiefly distin- 
guished by the presence of necrotic lesions in the spleen and liver. 

History. The disease has been described by a number of writers 
including Rieck, Wasielewski and Hoffman, Pfaff, Zwick, Miessner 
and Schern, Zeiss, and Binder. The last two writers independently, 
have thoroughly reviewed the literature of canary bird diseases. 
Doubtless the diseases observed by Kinyoun and by Ziirn are the 
same, and in the opinion of Zeiss the one observed by Kern is 
identical. On the other hand, Binder withholds decision as to 
whether or not Kern's disease is really the one in question. Most 
of the writers have refrained from giving the disease a name, but 
Miessner and Schern suggested the name infectious necrosis. 

Etiology. The organism causing the disease is a non-motile rod 
measuring from 1.5 to 2.5 microns long and .5 to 1. micron broad. 
Occasionally larger forms are observed. The organism is Gram 
negative and shows bipolar staining. Surface colonies on agar are 
grayish in color, appear distinctly granular and are about the size 
of a pinhead. 'No growth occurs on plain potato, but when this 
medium has been rendered alkaline a slight brownish colored layer 

252 



INFECTIOUS DISEASES OF CANAEY BIRDS 253 

forms. Bouillon becomes slightly clouded and abundant sediment 
accumulates. Milk is not coagulated and no gas is formed in sugar 
agar. Gelatin is not liquefied. Blue colonies form on Drigalski 
plates. A trace of indol was observed by one writer. 

Several writers who have worked with the organism regard it 
as a member of the hemorrhagic septicemia group. Miessner and 
Schern name the organism Bacillus canariensis necrophorus. 

Pathogenicity. The organism induces disease in canaries when 
introduced subcutaneously and per os. The disease must progress 
for at least three days in inoculated birds before the characteristic 
necrotic lesions develop. Mice, sparrows, finches, guinea pigs and 
rabbits are also susceptible. Pigeons vary in susceptibility while 
hens are resistant. 

Symptoms. There is nothing characteristic about the behavior 
of birds harboring this infection. The birds lose appetite, become 
less lively and finally squat in a corner of the cage. Death occurs 
after a sickness of from 24 to 36 hours. 

Morbid anatomy. The characteristic feature observed at 
autopsy is the presence of metastatic foci in the spleen, liver and 
occasionally in other organs. 

The liver is enlarged and contains numerous yellow foci the size 
of a pinhead and larger as seen by the unaided eye. The use of a 
hand lens reveals smaller punctiform foci. These areas present a 
great variety of shapes, and do not separate readily from the sur- 
rounding tissue. They are sometimes leathery in texture, some- 
times crumbly in structure. The larger ones when cut, are seen to 
consist of a homogeneous central mass surrounded by an opaque, 
gray colored zone. 

The spleen is swollen into a cylindrical form and contains similar 
nodules. These distend the capsule and cause the surface of the 
organ to have an irregular, undulating appearance. The spleen 
contains so many nodules and is so fragile in consequence, that it 
breaks apart when grasped with tweezers. The mucous membrane 
of the pharynx occasionally contains yellowish nodules which may 
be detached with the tweezers. The walls of the pleural cavities oc- 
casionally are covered with yellowish exudate, and the lungs may be 
involved. Intestinal inflammation is sometimes observed. 

The necrotic lesions closely resemble those of avian tuberculosis, 
but tubercle bacilli are not demonstrable. 

Stained sections of the nodules in the organs reveal the fact that 
the smaller ones consist of gi'eat clumps of bacteria which have 



254 DISEASES OF DOMESTICATED BIEDS 

multiplied at the places in question. The larger ones consist of 
clumps of bacteria surrounded by necrotic cells. The largest 
nodules consist of a number of smaller ones united together. 

The presence of the organism in the heart blood is not always 
demonstrated microscopically or by culture. 

Diagnosis. The disease can be recognized only by the char- 
acteristic lesions observed at autopsy. 

Treatment. No medical treatment is available. 

Prevention. General sanitation and isolation as recommended 
in paratyphoid B infection is suggested. 

INFECTION IN CANARIES CAUSED BY B. PAKATYPHOSUS B 

Synonyms. Septic fever in cage birds. 

Characterization. The disease is characterized by enlargement 
of the spleen with enteritis and is caused by B. paratyphosus B. 

History. The disease was described by Joest in 1906 and has 
been encountered later by Gilruth, Pfeiler, Adam and Medler, Man- 
ninger and by Binder. The latter writer and also Zeiss have sum- 
marized the work of earlier students of canary bird infections. 

Etiology. The organism isolated from the birds is a short 
plump rod 2 to 4 microns long and /^ to 1 micron broad with 
rounded ends. It is actively motile and Gram negative. Flagella 
may be demonstrated by Loffler's method, but wuth all care, it is pos- 
sible to demonstrate one flagellum only on the end of the rods. The 
organism in fresh smears from heart blood or organs often shows 
bipolar staining. 

Growth on agar, gelatin, bouillon, blood serum and potato is the 
same as that of cultures of B. paratyphosus B and B. supiestifer. 
Neither can differences be discovered between the growth of these 
cultures and the canary strains on Drigalski and Conradi or on 
Endo's fuchsin agar plates. 

In all strains, milk becomes brightened and yellowish colored 
after 8 days. After 14 to 20 days it becomes markedly yellow and 
transparent. After standing in the incubator for a longer time it 
becomes thickened, viscid and yellowish brown in color. Acid and 
gas are produced in dextrose, arabinose, rhamnose and zylose but not 
in lactose, saccharose, and raffinose. Indol is not produced. 

The organism agglutinates to B. paratyphosus B serum and para- 
typhoid B cultures of human origin agglutinates to serum prepared 
from the canary strain. 



INFECTIOUS DISEASES OF CANARY BIRDS 255 

Pathogenicity. The organism is highly virulent for canary 
birds, mice, guinea pigs and rabbits. 

Symptoms. In the beginning of the disease the bird is not so 
lively as usual and sits on the perches with ruffled feathers. Later 
the head is turned backward between the wings, which latter droop. 
Occasionally the bird hops about briskly and eats. As the disease 
progresses the bird becomes more depressed, appetite ceases en- 
tirely, the droppings become thin, the eyes are kept half closed and 
respiration becomes quickened to 150 per minute. Occasionally the 
bird peeps hoarsely. Movements become uncertain, the bird falls 
down, loses consciousness and dies in a spasm. 

Morbid anatomy. Rigor mortis is pronounced. The legs are 
most often extended from the body. There is more or less marked 
inflammation of the intestines. The spleen always shows hyperemic 
enlargement, twice to five times its normal size. There is 
hyperemia of the liver and kidneys. Smears from heart blood and 
organs, contain great numbers of short, thick rods in pure culture. 

Prophylaxis. The first measure should consist of separating 
the sound from the diseased birds. Further the healthy ones should 
be isolated in separate cages so far as possible. The droppings 
should be removed daily and be burned. Feed and water containers 
should be removed from the cages daily and be disinfected. 

Treatment. Sick birds may be supplied with drinking water 
containing 3 to 5 grams of sulphate of iron per liter. It is best to 
separate them so that there will be one or at the most two to a cage. 

DISEASE OBSERVED BY FREESE 

Freese has described a septicemic disease of canary birds sub- 
stantially as follows: 

Symptoms. The bird at first ruffles the feathers occasionally 
and is not so lively as usual. On the next day it sits quietly on the 
perch, peeps now and then and shows a certain degree of dyspnea. 
There is somewhat more thirst than usual but the appetite is not 
changed. In addition, there may be slight diarrhea. It is char- 
acteristic that the sick birds at frequent intervals hop around in the 
cage like healthy birds. The symptoms become more marked and 
the birds die in a day or so. Some hours before death they sit with 
ruffled feathers, on the perch or in the corner of the cage. The eyes 
are half closed and the head is turned backwards and held in the 
feathers. At this time there is a great increase in the frequency 



256 DISEASES OF DOMESTICATED BIEDS 

of respiration. It is noteworthy that the birds often continue to 
eat, up to a few hours before death. The duration of the disease is 
from two to three days. 

Morbid anatomy. The blood is coagulated and dark red in 
color. The mucosa of the duodenum is swollen and diffusely red- 
dened. The liver is either very much congested or fragile and yel- 
lowish in color. In most cases the spleen is without microscopic 
lesions but occasionally there is a hyperemic swelling of that organ. 

Etiology. In smears from the heart blood stained with the com- 
mon anilin dyes there are seen small rods 0.5 micron to 1.5 microns 
long which stain uniformly. In some cases an organism can only 
be found after long search. Bacteria are found very sparingly in 
smears from liver, spleen, and kidneys of fresh carcasses. In car- 
casses which have lain for several hours the bacteria are found in 
larger numbers. That these are not post-mortem invaders is shown 
by the fact that pure cultures of the organism in question may be 
obtained from such material. The organism is Gram positive in 
culture as well as in smears from tissues and is non-motile. It 
grows on all the common culture media at incubator and at room 
temperature but somewhat more slowly under the latter condition. 
The organism thrives best with access to air and less well anaerobi- 
cally. 

After twelve hours on slanted agar at incubator temperature the 
organism forms sharp bordered, distinctly prominent, shiny colonies 
about the size of a poppy seed. These are thickest in the center and 
become uniformly thinner toward the border. By reflected light 
they are grayish white in color. By transmitted light they are 
bright, transparent and have a bluish shimmer. On long standing 
these colonies do not become larger and do not change in appearance. 
Such isolated colonies develop after a light seeding of material such 
as heart blood from a fresh carcass. After rich seeding of material 
and after transfer from a culture a more uniform layer forms, espe- 
cially in the vicinity of the condensation water, which however, by 
close examination is seen to consist of colonies shaped like fine dew 
drops. After about twenty hours, growth ceases. At room tem- 
perature, growth is observed after twenty hours and stops at about 
thirty-six hours. 

The organism grows in a similar manner on four per cent glycer- 
ine agar, one per cent glucose agar, and on blood serum. On the 
latter medium growth appears first after twenty-four hours at in- 
cubator temperature and continues about three days. After this 



INFECTIOUS DISEASES OF CANARY BIRDS 257 

time there has fomied a very shiny, thin layer, the border of which 
appears finely toothed. 

The organism remains living on agar for six weeks without trans- 
ferring and on blood serum for eight weeks. 

On agar plates after fourteen hours at incubator temperature 
there are formed sharply defined, gray-white colonies about the size 
of a poppy seed which lie partly on the surface and partly within the 
medium. They do not change in appearance after a longer time. 

On gelatin plates one observes with the unaided eye, after forty 
hours, fine gi-ay-white points. By reflected light under the micro- 
scope with low magnification colonies are seen to have a brownish 
yellow color, have sharp borders and are circular or oval in form. 
In the center of these are a number of dark brown granules and on 
this account the center appears darker than the periphery. After 
two days a bright, transparent area forms about each colony and 
after three days one observes distinct liquefaction. This advances 
until the whole plate is liquefied after five days, reckoned from the 
time that the culture was planted. Similar gTOwth is observed on 
one per cent glucose gelatin plates. 

On slanted gelatin a distinct liquefaction occurs along the line of 
inoculation after forty-eight hours. On the bottom of the tube there 
is observed a large amount of cloudy fluid which has run down from 
the surface of the gelatin leaving a trough-like depression. In 
gelatin stab cultures after forty-eight hours punctiform colonies are 
observed along the line of the stab. There is a depression on the 
surface the size of a pinhead, which represents the beginning of 
liquefaction. 

The liquefaction progresses and in about fourteen days the whole 
of the medium becomes liquefied. Then there is observed a gray- 
white viscid mass in the bottom of the test tube which when shaken, 
ascends and forms a dense cloudiness. The organism remains alive 
on gelatin without transfer for about six weeks. 

In bouillon in the incubator after fourteen hours, the organism 
causes a uniform clouding and on shaking, a viscid sediment rises. 
The clouding continues till the third day and the sediment increases 
at the same time. After five days the upper part of the bouillon be- 
comes somewhat more clear and after fourteen days it becomes en- 
tirely clear. In the bottom of the test tube at this time there is an 
accumulation of brownish gray, thick sediment which on whirling 
the tube appears granular and stringy. No pellicile forms on the 
surface of the bouillon. Similar growth is observed in glycerine 



258 DISEASES OF DOMESTICATED BIEDS 

bouillon and in glucose bouillon. At room temperature growth in 
bouillon is somewhat more slow. The organism remains alive in 
bouillon for about four weeks. 

After 18 hours, growth occurs on potato in the form of prominent, 
sharply outlined grayish-white colonies about the size of a poppy 
seed. In the middle of the inoculated area these coalesce into a 
uniform layer. After two or three days the culture frequently be- 
comes brownish yellow in color in the thicker parts. The organism 
grows on potato at incubator and at room temperature equally well, 
and remains alive on this medium for six weeks. 

In whole milk at incubator temperature after 15 hours a marked 
separation of the whey occurs. The casein is coagulated in large 
flakes. After 36 hours the coagulation process is completed. At 
room temperature coagulation occurs first at 32 hours. In spite of 
the lactic acid, the organism remains alive four weeks without 
transfer. 

The organism forms no gas in the culture media employed and no 
acid, with the exception of that formed in milk. It develops no 
specific odor. 

Indol is not detected in bouillon cultures four days old. 

It is to be noted that in general the organism, in fresh cultures 
on the various media has the same form. In these, however, it 
appears shorter than in smears from tissues. Occasionally short, 
plump rods and very rarely, division forms occur. Among these 
may be observed many which are similar to a diplococcus. The 
organism appears somewhat smaller on blood serum than upon the 
other media. The organisms when grown on potato are the largest 
and longest. 

Pathogenesis. Hens, pigeons, rabbits and guinea pigs are in- 
susceptible to subcutaneous injection of culture or to injection of 
heart blood of a canary bird dead of the disease. In these birds 
it causes only a straw yellow focus about the size of a pea, at the 
point of injection. 

The infection may be transmitted to canary birds by inoculation 
and by feeding. Sparrows and mice are also susceptible. 

Freese compares the disease found by him with fowl cholera and 
with the diseases described by Kieck, Kern and Pfaff. He con- 
cludes that it differs from all of them. The one described by Kern 
shows the greatest similarity. The two practically agree in symp- 
toms, lesions and pathogenesis, but cultural characters show some 



INFECTIOUS DISEASES OF CANARY BIRDS 259 

marked differences. 'No subsequent writer seems to have encoun- 
tered the disease described by Freese. 

SEPTIC ENTERITIS OF CROSS BILLS 

Tartakowski has described a disease occurring in cross bills (Loxia 
curvirosa and pityopsittacus) , gold finches (Carduelis elegans), 
green finches (Chrysonitris spinus) and rarely in canary birds. 

Symptoms. The bird exhibits periods of dullness alternating 
with periods of apparent complete health. There are frequent at- 
tacks of weakness, somnolence with impairment of appetite, and in- 
creased thirst. The disease causes death in from 10 to 12 days. 
During the last few days the bird sits on the bottom of the cage 
with eyes closed. 

Morbid anatomy. When the disease has been of long duration 
the carcass shows great emaciation. There are no ecchymoses or 
exudates in the serous cavities. The breast muscles are always 
yellow as if cooked. Spleen and liver are always enlarged. Kid- 
neys and heart muscle are yellow and clouded. Earely there is 
marked hyperemia of the intestinal canal. Organs of respiration 
are normal. The brain is anemic. 

Etiology. There is constantly found in the spleen, liver and 
blood a rod which measures from 2. to 2.5 microns long and varies 
from .6 to 1. micron thick. The organism is actively motile and 
Gram negative. There is nothing distinctive about the growth on 
agar and gelatin. Gas formation occurs. There is no liquefaction 
in the latter. Milk is not coagulated. Tartakowski has designated 
the organism as Bacillus loxiacida. 

Pathogenesis. The organism is fatal to cross bills when ad- 
ministered in drinking water, and when injected subcutaneously or 
intramuscularly. In guinea pigs a local swelling is induced at the 
point of inoculation together with transient fever. Intraperitoneal 
inoculation causes a sero-fibrinous peritonitis and death in from one 
to two days. Rabbits injected the same way do not always die from 
peritonitis. 

REFERENCES 

1. Adam u. Medler. Ueber Paratyplins-B-Infektionen bei Kanarien- 
vogeln und Untersuchim^en iiber das Vorkommen von Bakterien der Koli- 
Typhusgruppe im normalen Kanarienvogeldarm. Centralhl. f. Bal'teriol. 
(Etc.), Orig., Bd. 62, 1912, S. 569. 



260 DISEASES OF DOMESTICATED BIRDS 

2. Binder. Ueber die infektiose Nekrose der Kanarien. Wien. tierdrztl. 
Wchnschr., Bd. 1, 1914, S. 337. 

3. Gray. Disease in canaries. Vet. Rec, Vol. 22, 1910, p. Y53. 

4. Gilruth. Diseases of canaries. Vet. J., n. s. Vol. 17, 1910, p. 655. 

5. Joest. Eine durch Bakterien der Enteritisgruppe verursachte 
Kanarienvogelseuehe. Ber. ii. d. Jc. Hochschule zu Dresden, Bd. 1, 1906, 
S. 110. 

6. Kern. Eine neue infectiose Ivrankheit der Kanarienvogel. 
(Kanariencholera) Deutsche Ztschr. f. Tiermed., Bd. 22, 1896, S. 171. 

7. Kinyoun. Vogelpest. Preliminary note. Centralhl. f. Bakteriol. 
(Etc.), 1 Aht. Orig., Bd. 38, 1906, S. 329. 

8. Miessner i\. Schern. Die infektiose Nekrose bei den Kanarienvogeln. 
Arch. f. TierheilK Bd. 34, 1908, S. 132. 

9. Pfaif. Eine infektiose Erkrankung der Kanarienvogel. Cen-tralU. 
f. Bahteriol. (Etc.), 1 Aht. Orig., Bd. 38, 1905, S. 275. 

10. Manninger. Ueber eine durch den Bacillus paratyphi B. verursachte 
Infektionskranklieit der Finken. CentralU. f. Balcteriol. (Etc.), Bd. 70, 
1913, S. 12. 

11. Pfeiler. Ueber ein seuehenhaftes, durch Bakterien aus der Para* 
typhusgruppe verursachtes Kanariensterben. Berl. tierdrztl. Wchnschr., 
Bd. 27, 1911, S. 953. 

12. Rieck. Eine infectiose Erkrankung der Kanarienvogel. Deutsche 
Ztschr. f. Tiermed., Bd., 15, 1889, S. 68. 

13. Tartakowski. Ueber eine Infektionskrankheit der Kreuzschnabel und 
anderer Zimmer-und Singvogel. Arch. d. Veterindrwesenschaften, 1898. 
(Russian.) Abstracted in Centralhl. f. BaUeriol. (Etc.), 1 Aht. Orig., 
Bd. 25, 1899, S. 89. 

14. Wasieliewski u. Hoffmann. Ueber eine seuchenhafte Erkrankung bei 
Singvogeln. Arch. f. Hyg., Bd. 47, 1903, S. 44. 

15. Zeiss. Beitrag zur Frage der Erreger von Kanarienvogelseuchen. 
Arch. f. Hyg., Bd. 82, 1914, S. 1. 

16. Zwick. Untersuchungen liber eine Kanarienvogelseuehe. Ztschr. f. 
InfeMionshr. d. Eaustiere., Bd. 4, 1908, S. 33. 



CHAPTER XXI 

TUMORS IN FOWLS 

Tumors in fowls hardly constitute a serious economic problem. 
However, in view of their great similarity in structure to those of 
man, they have received considerable attention. 

FREQUENCY OF OCCURRENCE OF TUMORS 

Curtis has reported upon the frequency of occurrence of tumors 
of fowls based upon autopsies of 880 birds. Of these 79, or 8^96 
per cent had tumors. This percentage corresponds to 90 cases of 
tumors per 1000 birds. 'No significant difference was noted in fre- 
quency of occurrence of tumors, between birds which died from nat- 
ural causes, and apparently normal birds which were killed. There 
is a sigTiificant correlation between age and the occurrence of tumors. 
Of the birds under 2^ years of age, only 7.37 per cent had tumors, 
w^hile they were present in 19.17 per cent of birds over that age. 
In birds which died from natural causes, and showed tumors, these 
were directly or indirectly the cause of death in from one-third to 
one-half the cases. There was a decided tendency for the associa- 
tion of hypertrophy of the liver, spleen or kidney, with the presence 
of tumors in other organs. The hypertrophy was apparently due to 
cell infiltration. Death often resulted from internal hemorrhage 
originating in the tumor, the underlying tissue or the hypertrophied 
liver or spleen. Data as to the character of the tumors were classi- 
fied with reference to whether the tumors were cystic or of solid 
tissue structure. Those of cystic structure comprised 22.78 per 
cent and solid tumors constituted 74.68 per cent. Three cases fell 
in both classifications in that cysts were attached to solid tissue 
tumors. In females the genital organs were most frequently in- 
volved. In 37.76 per cent of all, the tumors were in the ovary and 
18.36 per cent involved the oviduct and oviduct ligament. Too 
few males were examined to warrant drawing conclusions. In most 
cases the tumors were confined to one organ. In 15 cases metastasis 
had evidently occurred since tumors of similar nature were found 
in from two to four organs. 

261 



262 DISEASES OF DOMESTICATED BIKDS 

Ehrenreich collected data on the frequencj of the occurrence of 
tumors in fowls. Arrangement was made with a hotel to have sent 
to him the organs of all birds noticed to contain tumors. From 
nearly 2000 mature hens he obtained 7 malig-nant tumors of which 
5 were surely carcinomata. Doubtless the hotel employees over- 
looked many small tumors. It should be noted that the birds ex- 
amined were in apparent health and the discovery of carcinomata 
was purely accidental. Under more favorable conditions, the per- 
centage of carcinomata would have been higher. Among 3000 
pullets under a year old, no carcinomata were found, which confirms 
the belief that carcinoma is associated not with youth, but with 
maturity. 

CARCINOMA 

One carcinoma described by Ehrenreich was about the size of a 
hazel nut and had developed between the gizzard and the spleen. It 
was in contact with the upper end of the small intestine which 
showed stenosis at that point. The consistency was soft, the surface 
uneven and covered with shiny serosa. The color was gray and on 
section showed a few yellow points. Microscopic examination 
showed the tumor to be an adeno-carcinoma. 

Two more highly differentiated adeno-carcinomata were obtained 
from the ovary. They were about the size of a small apple or a 
man's fist, were of solid consistency, had rough surfaces and were of 
a reddish gray color. In both cases a seeding of small metastatic 
tumors on the peritoneum had occurred. 

Ehrenreich and Michaelis described three malignant tumors of 
the hen, of which two were adeno-carcinomata and one was a sar- 
coma-like tumor. 

SQUAMOUS CELL CARCINOMA 

Pick described a squamous cell carcinoma located beneath the 
floor of the mouth of a hen and which caused a marked deforma- 
tion of the region. The subject was a hen about seven years old. 
The tumor was observed at !N"ew Year's as a small lump and by 
September had grown to a mass measuring 4 by 3 by 3 cm. when the 
bird was killed. The tumor was located in the rear half of the floor 
of the oral cavity and bulged out on each side. It extended down- 
wards to the sparsely feathered area between the wattles. The sur- 
face was smooth except for a small ulcerated spot near the beak. 
On section it was observed that the tumor was necrotic near the 



TUMOKS IN FOWLS 263 

mouth cavity. Microscopic examination showed the tumor to be a 
typical squamous cell carcinoma. 

Koch describes a squamous cell carcinoma (cancroid) of a hen. 
The subject belonged to the Brahma-Putra breed, which is noted for 
its longevity. The bird had been in the Berlin Zoological Gardens 
for seven years and was full grown when brought there. Thus it 
was concluded that the bird must have been at least eight years old. 
The tumor was located in the roof of the oral cavity close to the back 
wall of the pharynx. It is to be noted that the other squamous cell 
carcinoma reported by Pick was located on the floor of the oral 
cavity and occurred in a seven year old hen. 

According to Koch's description, the internal organs present no 
noteworthy features. On opening the oral cavity by a cut through 
the left commissure of the beak there is revealed a somewhat solid 
mass which completely fills the pharnyx and exerts such pressure on 
the larynx that it contains a depression corresponding to it. The 
surface of this yellowish mass is spotted with bright red blood clots 
which may well have caused death by strangling. 

The yellow mass is so large that the disfigurement of the tracheal 
region would have been discovered in life but for the fact that it 
was covered with feathers. The tumor is very lightly attached and 
can be raised easily. It involves only soft tissue and no alteration 
of bone is observed. Microscopic examination shows the tumor to 
be a typical squamous cell carcinoma. 

CYSTO-ADENOMA 

Pickens has reported upon a cysto-adenoma in a fowl. The sub- 
ject was a rather large Plymouth Rock and appeared to be in rela- 
tively good condition. The abdominal cavity was found to con- 
tain a pint of very thin straw colored fluid. After being collected in 
a flask, and after standing, a small amount of sediment was precipi- 
tated. The proventriculus, gizzard, liver, spleen, intestines and 
peritoneum were covered with numerous white lobulated tumor-like 
masses. These varied greatly in size, some measuring 1-2 mm. in 
diameter while others measured 5 to 6 cm. in diameter. They were 
either sessile or attached to the serosa by means of a very short 
stalk. The stalk seemed to be a continuation of the capsule of the 
nodule, and was easily broken, leaving the tumor free. The capsules 
of the nodules were smooth and resembled the peritoneum very 
closely. Many of the larger of these nodules contained small sacs 



S 



264 DISEASES OF DOMESTICATED BIEDS 

or cysts attached to them. The cysts contained a small amount of 
serous fluid similar to that found in the abdominal cavity. Only 
one cyst occurred on a nodule. The proventriculus and gizzard 
showed only a few nodules. These were small varying from 2 mm. 
to 2 cm. in diameter. "No cysts were found on the nodules of these 
organs. 

Only a few nodules were attached to the liver and spleen. Those 
on the spleen were of the smaller variety and did not show cysts. 
There were several large nodules on the liver, the largest one meas- 
uring 6 cm. in diameter and contained a cyst. The stalk of this 
tumor seemed to extend down through the capsule into the liver 
tissue proper. The serous coverings of the small and large intestines 
were affected alike and showed the attachments of many tumors 
of varying size. Section of a medium sized nodule showed it to 
contain several cysts containing thin, straw colored fluid. The cut 
surface of the tumor was white in color, tinged with pink. It was 
firm in consistency and numerous blood vessels were seen. 

Histological examination of the tumors shows them to be made up 
of rather loose fibrous connective tissue stroma, relatively scarce in 
cells. Scattered irregularly through the stroma, and occupying 
approximately one-fourth of the area of the tumor are numerous 
alveoli, varying in size from a solid cord made of two or three 
epithelial cells to large cysts 5 mm. in diameter, in the larger 
nodules. The alveoli are lined with epithelium which range from 
squamous to columnar in type. The alveoli vary greatly in shape. 
Some are irregularly oval, while others are much elongated and com- 
paratively narrow, resembling the duct of a gland. Still others are 
found where numerous branching has taken place, giving the tumor 
the appearance of a papillary adenoma. The epithelium is, as far 
as can be determined, attached to a very thin basement membrane 
and the cells are only one layer thick. The connective tissue stroma 
of the tumor is exceedingly well supplied with blood vessels. The 
serous covering or capsules of the tumors are composed of rather 
dense fibrous connective tissue, which serves as the connection of 
the tumor to the serosa of the intestine. At the point of contact of 
the tumors with the liver, the liver cells have been replaced to a con- 
siderable extent with connective tissue stroma like that of the 
tumor. 



TUMOKS IN FOWLS 265 



FEATHEK CYSTS 



Koch observes that feather cysts (cystomata pennifera) occur in 
hens and geese, which are analogous to the dermoid cysts of mam- 
mals. 



LYMPHOMA 



Tyzzer and Ordway observe that lymphomata occur both with and 
without lymphatic leukemia. They regard the latter condition as 
due to the presence in the circulating blood of tumor cells having 
the characteristics of the cells of the lymphoid series. The only dis- 
tinction made by them between a leukemic lymphoma and lymphoma 
with lymphatic leukemia is that in the former the tumor is ex- 
travascular while in the latter the tumor is intravascular. Tumors 
observed by them occurred as definite primary growth either with or 
without secondary nodules or were so disseminated that the site of 
origin could not be determined. Some of the tumors have a more 
or less alveolar structure while others grow diffusely by infiltrating 
normal structures. Examples are given of a few cases observed by 
Tyzzer and Ordway. 

Lymphoma associated with lymphatic leukemia. Lympho- 
matous tumors are disseminated throughout the liver, the kidneys 
and the peritoneum; lymphatic leukemia. The subject is a hen at 
least one and possibly two years of age. The liver is greatly en- 
larged and presents many distinct rounded nodules of pale pink 
color distributed through its substance. Many of these nodules are 
apparent in the surface of the liver. Some present slightly de- 
pressed central areas, and elongated rounded borders. The largest 
measures 3 cm. across. The spleen is several times its normal size 
and is rather soft. The cervical lymph glands are enlarged. The 
kidneys are enlarged and studded with rounded pink nodules, some of 
which are 4 mm. in diameter. Distributed over various portions of 
the peritoneal surface are elevated plaques of tissue from which 
small blood vessels radiate into the surrounding normal tissue. 

The tissue of this case being poorly preserved it is impossible to 
determine the finer histological features of the cells. It is apparent, 
however, that the nodules in the liver, the kidneys, and the peri- 
toneum are composed of cells somewhat larger than the lymphoid 
cells of the circulating blood of the fowl and possess a more or less 
spherical, eccentrically situated nucleus. They correspond quite 
closely in their morphology to the plasma cell, and are evidently 



266 DISEASES OF DOMESTICATED BIEDS 

closely related to cells of the lymphoid series. The blood found in 
the vessels of various organs and tissues contains large numbers of 
these cells, so that the proportion of white cells in the circulating 
blood is very gTeat. In addition to the nodules of tumor tissue 
found in the liver and kidneys, these organs are to a large extent 
infiltrated with tumor cells. 

A case of lymphoma of the neck with metastasis to the lungs and 
the liver without lymphatic leukemia is described by the same 
writers. The cervical tumor appears as an oval flattened mass with 
an elevated rounded edge and a thick central crust. It measures 5 
by 6 cm. across and 2 cm. in thickness. On section it is found to be 
composed of rounded cells which vary considerably as to size, and 
which contain rounded, somewhat irregular nuclei. The liver is 
greatly enlarged. The right lobe presents a rounded nodule, 1 cm. 
in diameter consisting of tissue of similar appearance to that of the 
primary tumor. The entire liver is infiltrated with this tissue 
which appears to augiiient the size of the lobules and in places grows 
diftusely in areas 2 to 5 mm. in diameter. The tumor involves both 
lungs, and only a small portion of one lung contains air. ]^ear the 
roots of the lungs are two rounded nodules of tumor tissue. The 
tumor consists of cells with little supporting tissue. The latter 
consists for the most part of a delicate reticulum of connective tissue 
which apparently does not develop to any considerable extent within 
the tumor, but represents preexisting tissue into which the tumor 
has grown. There are also a few coarser bands of fibrous tissue. 
The tumor is rather vascular throughout, and the connective tissue 
reticulum is more distinct around the vessels than elsewhere. The 
tumor cells vary in size. Many are no larger than the lymphocytes 
of the circulation but some are equal in size to large connective tissue 
cells. They are apparently not concerned in the formation of in- 
tercellular fibrils. 

Another case reported presented a primary tumor of the nature 
of a Ij^Tiiphoma, situated on the neck, with secondary nodules on the 
sternum, in the lung and in the liver. The sternum and adjacent 
muscles are infiltrated with the tumor, but the tumor occurs as dis- 
crete nodules in the lung and liver. The spleen is not involved and 
the blood appears normal. 

Warthin observed several cases of leukemic Ipnphocytoma in 
fowls in which there were observed tumor-like nodules and infiltra- 
tion of Ij-mphoid cells in all the organs, particularly in the liver, 
spleen, kidneys, bone marrow, and hemolymph nodes. He observes 



TUMOKS IN FOWLS 267 

that aleukemic and leukemic forms of lymphocytoma occur and is 
of the opinion that the two conditions appear to be genetically re- 
lated if not different stages of the same process. He interprets the 
two conditions as malignant neoplasms. 



LEIOMYOMA 

Tyzzer and Ordway describe a leiomyoma of the mesentery of a 
hen. The specimen consists of a loop of hypertrophied intestine 
30 cm. long and 3 to 4 cm. in circumference. Within the mesentery 
and covered on both sides by peritoneum is a large rounded tumor 
of firm, flesh-like consistence, which measures 7 by 5 by 5 cm. This 
is of a general reddish pink color. On section the coloring is simi- 
lar, and the surface is traversed by firm, glistening bands of some- 
what lighter color. On scraping the surface, these stand out 
prominently and no soft tissue comes away. Between this tumor 
and the intestine is a tumor mass of similar character measuring 
2 by 1.5 cm. On histological examination the tumor is found to 
be composed of typical smooth muscle fibers running in various 
directions. Sections stained by the Van Gieson method for con- 
nective tissue show only a few small strands of fibrous tissue be- 
tween the masses of smooth muscle fibers. The tumor is composed 
chiefly of smooth muscle fibers and is in many respects similar to 
the leiomyoma of mammals. 

OSTEOCHONDEOSARCOMA 

Rous, Murphy and Tytler have described an osteochondrosarcoma. 
The fowl bearing the original growth was a Plymouth Rock hen in 
good condition and apparently about a year old. On the lower 
portion of the keel of the sternum was an irregularly spherical mass, 
so s^onmetrically disposed that the keel passed almost through its 
center. The tumor measured 6.6 by 5.7 by 4 cm. The growth was 
smooth, nearly as hard as bone and the skin over it was slightly 
stretched but not firmly attached. The tumor was well encapsu- 
lated. In the gross specimen the sternal keel could be traced to 
the center of the growth, but here it was lost in a mass of red, 
spongy, bony tissue wdiich radiated from it for a distance of one to 
one and one-half cm. Peripheral to this, the tumor was hard and 
white with fine strands of opaque, fibrous tissue separating more 
translucent, homogeneous areas. 



268 DISEASES OF DOMESTICATED BIEDS 

Microscopically the capsule of the tumor was found to consist of 
fihrous connective tissue containing isolated muscle bundles. The 
growth itself was made up of a zone of what may be called pre- 
chondral tissue, enclosing and grading into a mass of hyaline carti- 
lage through which ran the sternal keel. From this latter numer- 
ous irregular, bony trabeculse radiated into the cartilage. 

A brief recapitulation of the microscopic obsen^ations indicates 
that the outermost, youngest zone of the tumor is made up of cells 
of fibroblastic type scattered sparsely in a collagenous intercellular 
substance. In its deeper portions this tissue is undergoing a trans- 
formation to cartilage, its cells taking the character of cartilage cells, 
while the ground substance becomes homogeneous and basic staining. 
The original tumor is well encapsulated, and seems nearly, if not 
quite, stationary. 

The growth is readily propagated in other birds by transplanting 
small bits of fresh, peripheral, neoplastic cartilage. By means of a 
trochar, the grafts are placed deep in the pectoral muscles. In 
growth resulting from the transplantation, cartilage is laid down, 
followed later by bone if the bird lives long enough. Death results 
from the tumor but rarely and in such instances the host gradually 
becomes emaciated. The tumor is not transferable to the pigeon. 

The growth may also be induced by the filtrate of a Berkefeld 
filter. The tumor tissue is ground up with sterile sand. The re- 
sulting mass is suspended in Ringer's solution at blood heat and 
centrifugalized to free from tissue fragments. The supernatant 
fluid is passed through a Berkefeld filter of fine enough grade to re- 
tain B. fluorescens-liquefaciens. The percentage of tumors caused 
by the injection of filtrate is considerably higher when sterile in- 
fusorial earth is included. This material apparently causes a cell 
derangement favorable to tumor formation. 

SPINDLE CELL SAKCOMA 

Rous observed a spindle cell sarcoma in a Plymouth Rock hen 
about fifteen months old. A large irregularly globular mass pro- 
truded from the right breast. It had developed slowly and without 
apparent involvement of the health of the host. The bird was 
anesthetized and nearly all of the growth was removed. When 
sliced it was found to have undergone a widespread coagulation 
necrosis at the center, but there was a rim of translucent, rather 
friable, yellowish pink tissue of glistening, finely striated surface. 



TUMORS IN FOWLS 269 

Autopsy of the bird reveals the presence of about 20 c.c. of a thin 
straw colored fluid in the peritoneal cavity. Attached to the lower 
margin of the liver, to the oblique membrane, and to the parietal 
peritoneum are many firm, pale yellow, ovoid globular nodules, the 
largest about 1 cm. in diameter. On section these resemble the 
nodule in the left breast, except that in them the necrosis is irregu- 
larly distributed. At the pelvic region, where several of the masses 
have coalesced, softening and necrosis are extensive. No growths 
are visible in the other organs. 

Microscopic examination of the tumor reveals it to be a spindle- 
celled sarcoma. In a typical section there are observed loose bundles 
of spindle cells coursing in every direction, and separated from the 
lesser blood vessels only by endothelium. Where such a bundle is 
cut transversely, the appearance is that of a group of round cells of 
varying sizes. 

Transplantation of the tumor was accomplished by the use of 
fowds from the small, intimately related stock in which the growth 
appeared originally. Young chickens were more susceptible than 
adults. Market fowls of similar variety proved insusceptible as did 
pigeons and guinea pigs. During the first four generations, the 
tumor remained true to type and was infiltrative and destructive. 
Metastasis to the heart was observed once. 

The tumor has been found to be transferable by the filtrate of a 
Berkefeld filter. 

Rous has shown that ultraviolet light rapidly kills the cells of this 
transplantable sarcoma of the fowl without notably injuring the 
etiological agent associated therewith. The Roentgen ray has little 
effect on either cells or agent. 

He observes that fowls manifest two sorts of resistance to the 
avian tumor, one directed against the implanted tumor cells as such, 
the other against the action of the etiological agent to cause a neo- 
plastic change. In the individual fowl the two resistances appear 
to be independent of one another, though they may exist together or 
may both be absent. A recognition of them will perhaps explain 
some features in the biology of other tumors. 

Rous and Murphy observe that variations have from time to time 
occurred in the structure and behavior of this tumor. After a long 
series of transfers the growth frequently gave rise to fatal hem- 
orrhages from its substance. In some of the later, rapidly gTowing 
tumors the cells tended to be spherical, showing only a very tardy 
and imperfect differentiation to the spindle form. A giant-celled 



270 DISEASES OF DOMESTICATED BIRDS 

form of the growth was sometimes met with. Despite their diversity, 
the tumors graded into one another and in the final analysis, all are 
to be considered as spindle-celled sarcomata. 

Attempts to obtain an action of the etiological agent upon cells 
other than those it usually affects have failed, as have attempts to 
bring about changes in the histology of the sarcomata by attenuating 
the agent. 

Some of the lesser morphological variations in the sarcomata are 
undoubtedly due to local conditions of the host, and of the more im- 
portant changes some have been associated with an increase in the 
malignancy of the growth. For others the determining conditions 
have yet to be discovered. On the whole the variations described are 
not more marked than those occasionally manifested by the trans- 
plantable mammalian tumors, and traceable to the changes in a single 
strain of tumor cells during their propagation in successive hosts. 
In mammals the ultimate reason for these changes is not known. 
In the case of the chicken tumor some of them are undoubtedly the 
expression of changes in the causative agent of the gTowth. 

Rous and Lange describe a spontaneous chicken sarcoma. The 
subject was a mongrel brown Leghorn hen which was rendered lame 
by swellings on the left. leg. The growth regarded as the primary 
one was located in the gizzard. It occupied nearly the whole right 
anterior portion of the organ and projected irregularly under a cover- 
ing of mesentery in which were located several small nodules. The 
mass was roughly spherical and was about 4.3 cm. in diameter. The 
tumor was surrounded by muscle and encroached on the gizzard 
cavity. The tumor had no capsule but was sharply defined by its 
pale pinkish white color as contrasted with the wine color of the 
muscle. The tumor was made up of many irregular, tightly com- 
pressed subdivisions separated by minute, irregular fissures, and 
bulged on the cut surface. A localized soft yellow area of necrosis 
was located to one side, but in general the growth was translucent 
and appeared sound though poorly vascularized. The liver was en- 
larged, congested and mottled with ill defined, pale areas. Two 
small stellate depressions making irregular gray areas in the paren- 
chyma, were located on the surface of the organs. These proved to 
be composed of tumor tissue. The other viscera appeared normal. 

An oblong smooth mass 4,5 by 3 by 3 cm. was located in the ex- 
tensor muscles of the left thigh. A similar one was located in the 
muscles below the knee. The upper mass was attached to the peri- 
osteum for about 2 cm. above the patella and also to the joint capsule. 



TUMOKS IN FOWLS 271 

A prolongation extended from it to the back of the joint. The lower 
growth was attached to the joint capsule but the bulk of it lay in the 
muscle. These growths were extremely firm, more so than the one 
in the gizzard. They were pinkish white in color and nearly blood- 
less. They consisted of finely striated tissue in part solid and in 
part divided into irregular lobuli, like the tumor in the gizzard. 
Some of the lobuli had a central, semigelatinous depression and in a 
lew the center was yellow, firm and opaque, evidently necrotic. The 
growths were not encapsulated and were poorly defined from the 
muscle sheaths, periosteum and tendons which they involved. 

The knee joint was full of translucent, gristly papillary pro- 
liferations attached to the capsule or joint surface. These were ex- 
tensions from the growths on the outer surface of the capsule. 
Within the lower end of the femur and lying in the red marrow was 
a translucent tumor mass about A cm. in diameter. Tumors were 
also located in the muscle of the chest wall near the ribs, in the an- 
terior muscles of the neck and elsewhere. 

Microscopically, the tumor was found to consist of spindle-celled, 
sarcomatous tissue fissured and subdivided by many flattened sinuses, 
and often intracanicular in its growth. 

Transplantation was carried through eight successive groups of 
fowls. The development of the first few series of transplantation 
tumors was very slow. They exhibited the histological structure of 
the original growth and showed the same tendency to form metastatic 
foci in the skeletal muscles. Later the tumor grew more rapidly 
and underwent a simplification of structure to that of a pure spindle- 
celled sarcoma. Plymouth Rock fowls proved to be quite as satis- 
factory hosts as the brown Leghorn breed in which the tumor oc- 
curred originally. The agent causing the tumor was capable of 
passing through a Berkefeld filter. 

Gorig reports multiple sarcomata in a Plymouth Rock hen about 
three or four years old. During life the subject displayed difficult 
breathing, was greatly emaciated as a result of difficulty in eating 
caused by two tumors, which hung from the lower side of the neck. 

There is a tumor the size of a pigeon's egg suspended from the 
neck below the wattles. It is located in the subcutaneous connective 
tissue, has a solid consistency and the surface appears finely rough- 
ened. The skin is for the most part attached only loosely to the 
tumor and only in a small spot is there a close union between the 
two. This is marked from without by an excoriated spot on the 
skin. The tumor measures 5 by 3^2 cm. It is gray white in color 



272 DISEASES OF DOMESTICATED BIEDS 

and the cut section lias a slight shiny appearance. There are ob- 
served whitish threads of connective tissue between which there are 
darker islands of tissue. Blood vessels seem somewhat scarce. 'No 
lesions are observed in the internal organs. Microscopic examina- 
tion leads to the diagnosis of small spindle-cell sarcoma. 

L-YMPHO SAECOMA 

Regenbogen has described a case of multiple sarcomata of the 
skin of a hen two years old. The subject is in good condition, dis- 
plays good appetite and is active. A number of tumors are located 
on the head, neck, and back. These are of various sizes ; one involv- 
ing the left eye is 4 cm. in diameter. The surface of this tumor 
is uneven. The center appears dark brown as a result of the pres- 
ence of scabs and crusts. The periphery of the tumor shows the 
color of the skin and is thrown up in a circular ridge. The tumor 
extends above to the comb, below to the ear wattle, forward to the 
corner of the mouth and deep in the orbit. The other tumors move 
freely within the skin and are sharply defined from surrounding tis- 
sues. On the cut surface they are gTayish white in color, smooth 
and fatty. The center of the surface of the larger tumors has under- 
gone an ulcerative degeneration. 

Microscopic examination shows round cells for the most part. 
Between these is a scanty and delicate reticular foundation struc- 
ture. The vessels appear throughout as thin walled canals between 
the cell masses. From this it is seen that the tumor is a small round 
cell sarcoma, for instance, a lymphosarcoma. 

Ziirn and Pauly have observed diffuse round cell sarcomata in the 
liver of hens, and Watson has reported upon a round cell sarcoma in 
the heart of a fowl. 

MELANOSIS 

Lewin described a case of general melanosis in a young slaughtered 
hen. The bird had coal black feathers, beak and legs. The comb 
was dark red, the tongue and oral mucosa, black. After removing the 
feathers, the whole body appeared bluish black, the musculature shone 
bright through the skin and after removal of the skin, appeared un- 
altered. The loose tissues between the muscle groups contained 
black patches of various sizes and shapes. After opening the body 
cavity the serous surface was observed to be completely black, as was 



TUMOKS IN FOWLS 273 

the intestinal canal. Black patches were present on the gizzard and 
heart. After removing the flesh from the bones, the periosteum was 
observed to be wholly black as were also the cartilages of the joint 
surfaces. After scraping the periosteum the bone was seen to be 
black in places. 

A specimen exhibiting generalized melanosis in a fowl is included 
in the pathological collection of the IsTew York State Veterinary 
College at Cornell University. 

MYXO-SARCOMA 

Tvzzer and Ordway describe a myxo-sarcoma of the thigh of a 
hen in part as follows. The tumor was situated on the outer aspect 
of the thigh of an adult hen, and appeared as a turban-shaped mass 
with a depressed central area and an elevated rounded edge. It 
measured 5 cm. across and 2 cm. in thickness. On section it was 
found to consist chiefly of a translucent, soft tissue almost gelatinous 
in consistence. The tumor is found to be composed of lobules of 
tissue which consist of cells widely separated from one another by a 
relatively large amount of intercellular material. The lobules are 
to a large extent limited by connective tissue which in places forms 
a definite capsule. In certain places, however, the tumor is without 
capsule of any sort and appears to be infiltrating the subcutaneous 
fat. The central portions of many of the lobules are necrotic, and 
the cells in the surrounding tissue are somewhat degenerated. The 
connective tissue around the lobules is loose and vascular in places, 
and, since .there is in such places a marked infiltration with leu- 
cocytes, it resembles closely granulation tissue. In it are found 
large numbers of lymphoid and plasma cells, and large phagocytic 
cells. 

The cells of this tumor present the characteristics of connective 
tissue cells, and are associated with intercellular material consisting 
in part of a fibrillar reticulum, in part of a homogeneous substance 
which reacts to staining reagents like mucin. The fibrillar material 
is probably closely related to collagin, although it is stained some- 
what atypically with alum hematoxylin. The tumor is malignant 
in that it is rapidly growing, and in that it infiltrates normal tissues 
such as fat and nerves. Although blood vessels of considerable size 
are found within many of the lobules, the tumor tissue is not every- 
where well vascularized, and is prone to necrosis. N'o metastases 
were found. 



274 DISEASES OF DOMESTICATED BIRDS 



MYXO-FIBROMA 

Koch observed tumors in a partridge which closely resembled 
avian tuberculosis. Both ceca were studded with numerous tuber- 
cules some as large as a pea. However the larger ones had a glazed 
appearance resembling cysts with gelatinous contents, while the 
smaller ones had an opaque, whitish gray appearance. Some of the 
larger tubercules showed a similar characteristic. Some of these 
were located in the intestinal wall protruding in the lumen as a 
hemisphere, without perforating the mucosa. 

Microscopic examination showed the large tubercles to be myxo- 
fibroma and the smaller ones to be a pure fibroma. 

REFERENCES 

1. Curtis. Frequency of occurrence of tumors in the domestic fowl. U. 
S. Dep. Agr. J. Agr. Research, Vol. 5, 1915, p. 397. 

2. Ehrenreich and Michaelis. Ueber Tumoren bei Hiilmern. Ztschr. 
Krehsforch., Vol. 4, 1906, S. 586. 

3. Ehrenreich. Weitere Mittheilungen iiber das Vorkommen malignes 
Tumoren bei Hiihnern. Med. Klin., Berlin, Bd. 3, 1907, S. 614. 

4. Gorig. IVfultiple Sarkome beim Hubn. Deutsche tierdrztl. Wchn- 
schr., Bd. 8, 1900, S. 54. 

5. Jones. A myxo-cbondro-carcinoma of the testicle of a fowl. Bept. 
N. Y. State Vet. College, 1912-1913, p. 160. 

6. Koch. Demonstration einiger Gescbwulste bei Tieren. Verhandl. 
Deutsche Path. GeseUsch., Bd. 7-8, 1904, S. 136. 

7. Lange. On certain spontaneous chicken tumors as manifestations of 
a single diesase. II. Simple spindle-celled sarcomata. J. Exper. M., Vol. 
19, 1914, p. 577. 

8. Lewin. Ueber einen Fall von allgemeiner Melanose beim Huhn. 
Ztsch. f. Veterindrh., Bd. 22, 1910, S. 455. 

9. Murphy and Rous. The behavior of chicken sarcoma implanted in 
the developing embryo. J. Exper. Med., Vol. 15, 1912, p. 119. 

10. Petit et German. Le cancer de I'ovaire chez la Poule. Bull. Soc. 
Cent, de Med. Vet.. T. 63, 1909, pp. 341 and 386. 

11. Pick. Zur Frage vom Vorkommen des carcinoms bei Vogeln: 
Grosser Plattenepithelkrebs des Mundhohlenbodens bei einem Huhn. 
Berl. Tclin. Wchnschr.. Bd. 40, 1903, S. 669. 

12. Pickens. A cysto-adenoma in a fowl. Bept. N. Y. State Vet. Coll., 
1913-1914, p. 261. 

13. Regenbogen. Multiples Sarkom in des Haut eines Hahnes. Berl. 
tierdrztl. Wchnschr., Bd. 19, 1907, S. 323. 

14. Rous. Resistance to a tumor-producing agent distinct from re- 
sistance to the implanted tumor cells. J. Exper. M., Vol. 18, 1913, p. 416. 

15. Rous. A transmissible avian neoplasm (Sarcoma of the common 
fowl). J. Exper. Med., Vol. 12, 1910, p. 696. 



TUMOKS IN FOWLS 275 

16. Rous. On certain spontaneous chicken tumors as manifestations of 
a single disease. I. Spindle-celled sarcomata rifted with blood sinuses. 
J. Exper. Med., Vol. 19, 1914, p. 570. 

17. Rous and Lange. The characters of a third transplantable chicken 
tumor due to a filterable cause. A sarcoma of the intracanicular pattern. 
J. Exper. Med., Vol. 18, 1913, p. 651. 

18. Rous and Murphy. Variations in a chicken sarcoma caused by a 
filterable agent. J. Exper. Med., Vol. 17, 1913, p. 219. 

19. Rous and Murphy. On the causation by filterable agents of three 
distinct chicken tumors. /. Exper. Med., Vol. 19, 1914, p. 52. 

20. Schlegel. Maligne Neoplasmen. Ztschr. f. tiermed., Bd. 17, 1913, 
S. 387. 

21. Tytler. A transplantable new growth of the fowl producing car- 
tilage and bone. J. Exper. Med., Vol. 17, 1913, p. 466. 

22. Tyzzer and Ordway. Tumors in the common fowl. J. Med. Re- 
search, Vol. 21, 1909, p. 459. 

23. Warthin. Leukemia of the common fowl. J. Infect. Dis., Vol. 4, 
1907, p. 369. 

24. Watson. Malignant disease of a heart of a fowl. Vet. J., Vol. 9, 
1904, p. 182. 



S 



CHAPTER XXII 

TOXICOLOGY 

It is a well established fact that considerable variations in toler- 
ance to drugs of a toxic nature exist in animals of different species. 
While these variations have been pointed out in the case of mam- 
malian species, little information is found in toxicologic literature 
on the toxicity to fowls of drugs or poisonous substances which may 
be of value in the treatment or control of avian diseases. 

The experiments described in this chapter were undertaken by 
Gallagher for the purpose of determining the toxic doses for 
fowls of the more commonly used medicinal agents and of poisonous 
substances to which fowls not infrequently have access. JSTo attempt 
was made to fix the toxic dose in certain instances where the sub- 
stance on test proved non-toxic when given in comparatively large 
quantities. A few tests only were made with each substance. The 
results of these are summarized in the doses indicated under the name 
of each drug. In a few instances reference has been made to obser- 
vations by other writers. 

In each experiment, unless otherwise stated, fluids were admin- 
istered directly into the esophagus or crop by means of a pipette and 
solids were given in gelatin capsules per os. 

Medium sized healthy mature hens weighing between 3 and 4 
pounds were usually employed. Those of larger size are designated. 
All doses were given while the crop contained a normal amount of 
food. 

From the results of the experiments it may be concluded that in 
general fowls may be considered as having approximately the same 
susceptibility to toxic substances as medium sized dogs. They are 
more resistant than dogs to such substances as calomel, strychnine 
and tartar emetic, and less resistant to carbolic acid, salicylic acid 
and potassium cyanide. 

In treating outbreaks of disease in fowls, it is of great advantage 
to employ the drinking water as a vehicle for medicinal agents. It 
is shown that fowls are not visibly affected by drinking solutions of 
bichloride of mercury 1-6000, carbolic acid 1-1000, permanganate 

276 



TOXICOLOGY 277 

of potash 1-500, and crude catechu 1-500 for periods of 18 to 21 
days. 

It is interesting to note that the crop not only serves as a reservoir 
for food, but that absorption through its wall is very rapid,- symptoms 
appearing in from two to five minutes after the administration of 
such substances as amnionium chloride in solution, potassium cy- 
anide and strychnine sulphate. 



AMMONIUM CHLORIDE 

Lethal dose. 60 grains. 

45 grains in solution (15 c.c. of 20 per cent so- 
lution). 
Toxic dose. Same as lethal. 
I^on-toxic dose. 15 to 45 grains. 

Experiments. (1) July 8, 1918, 2 p. m. Fowl received 60 
grains of ammonium chloride. July 9. Fowl droopy, weak in legs, 
sitting. July 10. Same as July 9. July 11. Fowl died before 

8 A. M. Autopsy notes. ]^o lesions were apparent. 

(2) February 20, 1918, 11.05 a. m. Fowl received 45 grains of 
ammonium chloride in 12 c.c. of water (15 c.c. of a 20 per cent solu- 
tion). Stimulating effect observed almost immediately. Fowl had 
not been very active previously. After administration of the chlo- 
ride, bird began scratching energetically and singing more than the 
neighboring untreated fowls. Would drop wing on one side in imi- 
tation of a rooster and would crowd up against the side of the cage 
which separated her from another hen. Would peck at her through 
the cage. 11.20 a. m. Same as above. 11.25 a. m. Drinking con- 
siderable water. 11.30 a. m. Excitement has passed. 1.00 p. m. 
Fowl has a sleepy appearance. Bunches up somewhat when not dis- 
turbed. 4.30 p. m. 'Not active. Bunched up. February 21, 1918, 

9 A. m. Fowl sleepy and bunched up. Stands erect but wabbles 
when disturbed. 4.30 p. m. Fowl droopy. Bunched up. Feathers 
ruffled. February 22. Above described condition intensified. Feb- 
ruary 23. Fowl died before 8 a. m. Autopsy notes. Crop filled 
with food. Lungs pale. Other organs apparently normal. 

(3) June 25, 1918, 10 a. m. Fowl received 45 grains of ammon- 
ium chloride. Result. No effect was apparent. 

(4) February 28, 1918, 10.05 a. m. Fowl received 15 gi-ains of 
ammonium chloride. Eesult. No effect was apparent. 



S 



278 DISEASES OF DOMESTICATED BIEDS 



AKSENIOUS ACID 

Lethal dose. 5 grains. 

Toxic dose. 5 grains. 

]Sron-toxic dose. 1 to 3 grains. 

Experiments. (1) June 10, 1918, 10 a. m. Fowl received 5 
grains of arsenious acid. 4.00 p. m. Fowl somewhat droopy. 
Droppings greenish. July 11, 9,00 a. m. Fowl droopy. Drop- 
pings greenish and watery. 12 m. Fowl weak. Comb dark. 
1.30 p. M. Fowl dead. Autopsy notes. Food in crop and gizzard. 
Catarrhal exudate in the proventriculus. Internal membrane of the 
gizzard is necrosed and separated from wall at entrance of pro- 
ventriculus. Contents of gizzard greenish. Duodenum shows a ca- 
tarrhal condition and is pale in color. Contents of intestines are 
fluid and of greenish tinge. Liver is mottled. Rigor mortis is 
marked 1 hour after death. 

(2) July 8, 1918, 2 p. m. Fowl received 3 grains of arsenious 
acid. Result. ]^o effect was apparent. 

(3) June 25, 1918, 10.00 a. m. Fowl received 1 grain arseni- 
ous acid. Result. No effect was apparent. 

Reinhardt fed .2 gram of arsenic and observed no symptoms up 
to the sixtieth hour. He then gave .4 gram more and the hen died 
40 hours after the last dose was administered. A second hen died 
(^Yo days after receiving .2 gram of arsenic. 

Reinhardt observes that arsenic poisoning in hens causes lesions 
which are characteristic with reference to location and character. 
The horny epithelial layer of the gizzard is raised from the under- 
lying muscles by a gelatinous or sero-fibrinous exudate and in con- 
sequence is easily peeled off. The exudate lying beneath the epi- 
thelium, in places reaches a thickness of 1 cm. Sometimes this 
exudate consists of a serous, yellowish, clear fluid, which spurts out 
when an incision is made in the tissues. In case the epithelial layer 
has been perforated, only a small amount of gelatinous exudate may 
be present. On removing the epithelial layer, highly reddened 
areas due to corrosive action, may be observed. The proventriculus 
shows no lesions. The mucosa of the crop is somewhat reddened, 
the vessels of the intestines are injected and the contents of the in- 
testines are thinly fluid. The liver is usually yellowish brown in 
color and fragile, due to fatty degeneration. The fat, especially on 
the gizzard is somewhat edematous and soft. Frequently the fat is 



TOXICOLOGY 279 

orange colored. The blood is well coagulated and brownish red in 
color. 

BICHLORIDE OF MERCURY (meRCURIC CHLORIDE, CORROSIVE 

sublimate) 

Lethal dose. 4 grains. 

Toxic dose. 4 grains. 

Non-toxic dose. 3 grains. 

1-6000 solution as drinking water for 18 days without harm. 

Experiments. (1) June 10, 1918, 10 a. m. Fowl received 5 
grains of bichloride of mercury. 10.45 a. m. Spasmodic move- 
ments of the crop for several minutes. 11.45 a. m. Droopy. 2 
p. m. Sitting. Legs weak. Drooping. 4 p. m. Sitting. Cannot 
stand. Marked depression. June 11, 1918, 9 a. m. Fowl found 
dead. Autopsy notes. 'No food in crop. Gizzard filled with food. 
Mucous membrane of dependent portion of crop is whitened and thick- 
ened as a result of coagulation necrosis. Proventriculus shows severe 
catarrhal condition. Mucosa at entrance to gizzard is necrosed. 
Membrane of posterior portion of gizzard is separated from the giz- 
zard wall, the space being filled with clear fluid. Mucosa of first 
third of intestine is exfoliated and remainder of small intestine shows 
a severe catarrhal condition. Other organs apparently normal. 

(2) August 12, 1918, 2.20 p. m. Four pound fowl received 4 
grains of bichloride of mercury. 4.30 p. m. No change noted. Au- 
gust 13, 9 A. m. Legs very weak. Bird cannot walk. Sits down. 
Otherwise looks bright and normal. August 14, 9 a. m. Fowl can- 
not stand. August 15, 9 a. m. Fowl dead. Autopsy notes. Small 
amount of oats in crop. Crop wall is thickened, pale; mucosa is 
coagulated. Subcutaneous tissue surrounding crop and esophagus 
is infiltrated with a greenish gelatinous exudate. Proventriculus 
shows several hemorrhagic points on mucosa. Gizzard contains a 
considerable quantity of gi-eenish colored food. Mucosa of small in- 
testine is pale. Kidney is very pale and studded with minute white 
spots. Air sac membranes in abdominal cavity are thickened. The 
abdominal cavity contains 6 ounces of a thick somewhat viscid fluid 
with a slight greenish tinge. 

(3) February 28, 1918, 10 a. m. Fowl received a tablet contain- 
ing 3 grains of bichloride of mercury and 3 grains of ammonium 
chloride. Result, No effect was apparent. 



280 DISEASES OF DOMESTICATED BIEDS 

(4) May 27, 1918, 10 a. m. Gave fowl 1.4 grains of bichloride 
of mercury in feed. Fowl had not been fed for 24 hours, crop nearly 
empty. 3 p. m. Gave fowl another 1.4 grains of bichloride of 
mercury in feed. Kesult. ISTo effect was apparent as a result of 
fowl consuming 2.8 grains of bichloride of mercury in feed in one 
day. 

(5) June 14, 1918. Gave three fowls a 1-6000 solution of bi- 
chloride of mercury as drinking water. Fowls drank solution for 
a period of 18 days consuming about 2500 c.c. each. 'No other 
water was given. Result. No effect was apparent. 

(6) June 12 to 14, 1918. Several fowls which had not received 
drinking water for 24 hours were given bichloride of mercury solu- 
tions of 1-2000 and 1-4000 as drinking water. Fowls tasted solu- 
tions and refused to drink. Solutions were clear. At intervals the 
solutions were again placed in the fowls' cages with the same result 
as above. After taking 1 to 3 swallows of solution the fowl shakes 
its head, rubs beak in the litter and elevates the feathers on the neck 
for a few moments. Gave fresh water and fowls drank eagerly. 

Ward, adopting a suggestion by Ritzier, employed corrosive sub- 
limate in the drinking water of a large flock of birds during an out- 
break of fowl cholera, without harmful result. The period during 
which the sublimate was used to disinfect the water covered 16 
days. For the first two days a solution of 1 : 1000 was employed. 
Since the fowls did not drink the solution readily, the bichloride was 
diluted to 1 part to 2000 parts of water. 

BISMUTH SUBNITRATE 

IS'on-toxic dose. /4 ounce -j- 

Experiment. (1) February 20, 1918, 9.50 a. m. Fowl received 
/4 ounce of bismuth subnitrate. Result, l^o effect was apparent. 

CALCIUM OXIDE ( QUICKLIME) 

Toxic dose. 1^4 drams. 

ISTon-toxic dose. % dram. 

Experiments. (1) August 15, 1918, 9.40 a. m. Gave 3 pound 
fowl 134 drams of calcium oxide. August 16. Fowl is somewhat 
droopy. Droppings are greenish in color. August 17. Fowl is 
dull in appearance. August 18. Fowl is dull in appearance. 
August 19. Fowl appears normal. 



TOXICOLOGY 281 

(2) August 27, 1918, 10.30 a. m. Gave 3% pound fowl V2 dram 
of calcium oxide. Result. No effect was apparent. 

CALOMEL (mEECURIOUS CHLORIDe) 

ISTon-toxic dose. 30 grains. 

Experiment. (1) February 7, 1918, 10,30 a. m. Fowl received 
30 grains of calomel. February 8, 9 a. m. Evidence of purging. 
Droppings greenish. Fowl has not been visibly affected otherwise. 

CARBOLIC ACID 

Toxic dose. 5 grains in solution (11 c.c of 3 per cent solution). 
3.75 grains in solution (12.5 c.c. of 2 per cent solu- 
tion). 

N"on-toxic dose. 2 grains in solution (13 c.c. of 1 per cent solu- 
tion). 

1-1000 solution as drinking water for 18 days. 

Experiments. (1) August 12, 1918, 2.20 p. m. Five pound 
fowl received 11 c.c. of 3 per cent carbolic acid solution (5 grains 
carbolic acid). 2.22 p. m. Crop puffed out somewhat. 3.00 p. m. 
Fowl has showm some droopiness since receiving the solution. 3.45 
p. M. Fowl apparently normal. 4.30 p. m. Fowl apparently nor- 
mal. August 13. Fowl appears normal. 

(2) February 2, 1918, 10 a. m. Three pound fowl received 12.5 
c.c. of 2 per cent carbolic acid solution (3.75 grains carbolic acid). 
11 A. M. Fowl shows dullness. 2 p. m. Fowl appears normal. 
February 3. Fowl is apparently normal. 

(3) AugTist 27, 1918, 10.30 a. m. Gave 4 poimd fowl 13 c.c. of 
1 per cent carbolic acid solution (2 grains carbolic acid). Result. 
"No effect was apparent. 

(4) June 14, 1918. Gave three fowls a 1-1000 solution of car- 
bolic acid as drinking water for a period of 18 days. Each fowl 
consumed about 2500 c.c. 'No other water was given. Result. ISTo 
effect was apparent in any of the fowls. 

(5) June 14, 1918. Several fowls were given carbolic acid solu- 
tions of 1-250 and 1-500 as drinking water. Fowls refused to 
drink the solutions. Gave fresh water and fowls drank eagerly. 



S 



282 DISEASES OF DOMESTICATED BIEDS 



CASTOR OIL 

Non-toxic dose. 6-J4 drams -j" 

Experiment. (1) February 7, 1918, 10.30 a.m. Fowl received 
634 drams of castor oil. February 8, 1918. 9 a. m. Evidence of 
moderate purging. Droppings greenish. Fowl was not visibly af- 
fected otherwise. 

CATECHU (crude) 

N'on-toxic dose. 1-500 solution + 

Experiment. (1) June 10, 1918. Gave fowl a 1-500 solution 
of crude catechu as drinking water. Fowl drank solution freely. 
July 1, 1918. Fowl drank 3000 c.c. of above solution in 21 days. 
No other water was given. 'No constipation was observed. No 
change in fowl was apparent. 

CHLORIDE OF LIME 

Non-toxic dose. % to 1/4 drams. 

Experiments. (1) August 15, 1918, 10.30 a. m. Five pound 
fowl received 1^4 drams of chloride of lime. Result. No effect 
was apparent. 

(2) August 13, 1918, 2.30 p. m. Five pound fowl received % 
dram of chloride of lime. Result. No effect was apparent. 

COPPER SULPHATE (bLUE STONe) 

Lethal dose. 20 grains. 

15 grains in solution. 

Toxic dose. Same as lethal. 

Non-toxic dose. 5 to 15 grains. 

Experiments. (1) July 8, 1918, 2 p. m. Fowl received 20 grains 
of copper sulphate. 4 p. m. No change apparent. July 9. Fowl 
droopy. Sitting. July 10. Same as July 9. July 11, 9 a. m. 
Fowl dead. Autopsy notes. Pharynx and esophagus show coagula- 
tion of the mucosa. Mucosa of crop exfoliated. Crop filled with 
water and greenish catarrhal exudate. Lower esophagus shows co- 
agulation necrosis of mucosa. Proventriculus shows severe catarrhal 
gastritis. Catarrhal enteritis. Entire intestine is filled with green- 
ish catarrhal exudate. 



TOXICOLOGY 283 

(2) February 2, 1918, 10 a. m. Fowl received 15 grains of cop- 
per sulphate in solution (10 c.c. of 10 per cent solution). Fowl 
drank water continuously for 15 minutes then became restless for 
about three minutes. 12 m. Dull. 2 p. m. Dull. 4.30 p. m. 
Dull. February 3, 1918, 9 a. m. Fowl is droopy. 9.30 a. m. 
Convulsions developed and fowl died. Autopsy notes. Crop nor- 
mal. Distended with water. Considerable food in crop and giz- 
zard. Mucosa of proventriculus intensely inflamed. Horny mem- 
brane of gizzard loosened near opening of proventriculus. Hem- 
orrhagic points in submucosa. Catarrhal enteritis is quite marked. 
Intestine contains considerable bluish fluid. Mesenteric fat and 
peritoneum are petechiated. Heart is in systole. 

(3) June 25, 1918, 10 a. m. Fowl received 15 grains of copper 
sulphate. Result. No effect was apparent. 

(4) February 28, 1918, 10.10 a. m. Fowl received 5 grains of 
copper sulphate, ivesult. I^o effect was apparent. 

ERGOT. F. E. 

!N"on-toxic dose. 2^ drams F. E. equivalent to 2/4 drams of ergot. 

Experiment. (1) February 8, 1918, 10.30 a. m. Fowl received 
2% drams of fluid extract of ergot with 2^ drams of water. Result. 
'No effect was apparent. 

FEKKOUS SULPHATE ( COPPERAS ) 

IsTon-toxic dose. 30 grains + 

Experiment. (1) February 7, 1918, 10.30 a. m. Fowl received 
30 grains of ferrovis sulphate in solution (10 c.c. of 20 per cent solu- 
tion). Result. No effect was apparent. 

IPECAC. F. E. 

Lethal dose. 1 to 2 drams. 

Toxic dose. 1 dram. 

Non-toxic dose. -!4 to % dram. 

Experiments. (1) August 19, 1918, 1.10 p. m. Gave 4^2 pound 
fowl 2 drams fluid extract of ipecac. August 20. No apparent 
change. August 21, 9 a. m. Greenish fluid droppings. August 22, 
9 A. M. Fowl dead. Autopsy notes. Crop and gizzard filled with 
food. Mucosa of crop pale, slightly thickened. Lower esophagus 



284 DISEASES OF DOMESTICATED BIEDS 

and proventriculus show a catarrhal condition. Several hemor- 
rhagic points in proventriculus. Small area of internal lining of 
gizzard at entrance of proventriculus separated from gizzard wall. 
Mucosa of duodenum pale. Liver pale. 

(2) August 19, 1918, 1.10 p. m. Gave 3 pound fowl iH drams 
fluid extract of ipecac. Aug-ust 20, 9 a. m. Fowl dead. Autopsy 
notes. Some food in crop. Proventriculus shows a catarrhal con- 
dition. Hemorrhagic near entrance to gizzard. Membrane of giz- 
zard easily separated near opening of proventriculus. Liver is 
banded with light and dark stripes. 

(3) August 27, 1918, 10.30 a. m. Gave 41/2 pound fowl 1 dram 
of fluid extract of ipecac. August 28. ]^o change apparent. 
August 29. Fowl dull. August 30. Fowl dead at 9 a. m. Au- 
topsy notes. Crop and gizzard filled with food. Mucosa of pro- 
ventriculus thickened and catarrhal. Submucosa of gizzard near pro- 
ventricular opening hemorrhagic. Liver pale in spots and streaked 
with darker bands. Heart in systole. 

(4) August 12, 1918, 2.20 p. m. Gave 5 pound fowl 1^/4 drams 
fluid extract of ipecac. August 14, 9 a. m. Fowl has shown no 
change. August 15. Somewhat dull. August 16. Same as Au- 
gust 15. August 17. Apparently normal. 

(5) August 30, 1918, 10.30 a. m. Gave 4 pound fowl % dram 
of fluid extract of ipecac. Eesult. JSTo effect was apparent. 

(6) August 30, 1918, 10.30 a. m. Gave 4 pound fowl ^A dram of 
fluid extract of ipecac. Result. ISTo effect was apparent. 

LEAD OXIDE (lITHAEGe) 

ISTon-toxic dose. iVi drams. 

Experiment. (1) August 15, 1918, 9.40 a. m. Five pound fowl 
received 1/4 drams of lead oxide. Result, l^o effect was apparent. 

MAGNESIUM. SULPHATE 

(Epsom Salts) 

iN'on-toxic dose. 1 dram in solution + 

Experiment. (1) February 7, 1918, 11 a. m. Fowl received 1 
dram of Epsom salts in 4% drams of water. February 8, 9 a. m. 
Evidence of moderate purging. Droppings fluid and brownish. 
Fowl was not visibly affected otherwise. 



TOXICOLOGY 285 



MALE FEKN. F. E. 

Toxic dose. 2^ drams, F. E. 

ISTon-toxic dose. 1-54 drams, F. E. 

Experiments. (1) April 25, 1918, 11.15 a. m. Fowl received 
2% drams of fluid extract of male fern. 11.30 a. m. Fowl sleepy. 
Droopy. 11.45 a. m. Fowl sleepy. Sittino;. 12 m. Legs very 
weak. 1 p. M. Very weak. Can raise itself on its feet with dif- 
ficulty. 2.45 p. M. Sitting, Has great difficulty in attempting to 
stand. 4 p. m. Standing but legs are still weak. April 26, 1918, 
9 A. M. Fowl has recovered. 

(2) July 8, 1918, 2 p. m. Fowl received 1^ drams of fluid ex- 
tract of male fern. Result. IsTo effect was apparent. 



PHOSPHORTTS 

Poisoning with this substance may occur as a result of eating rat 
poison. The writers have observed a case of phosphorus poisoning 
induced by eating the debris left after a display of fireworks among 
which was fine gravel employed in " torpedoes." 

Birds exhibit depression, weakness, trembling, diarrhea, thirst 
and sometimes emphysema of the skin. Death may occur within a 
period varying from one hour to several days. 

At autopsy, care should be taken in opening the crop, proven- 
triculus and gizzard in looking for the so-called phosphorus vapor 
which appears as a transient cloud on opening the organs or when the 
contents are moved. The phosphorus in the crop and gizzard may 
be detected by the characteristic odor and by faint luminosity when 
in the dark, especially if the material is rubbed. The more pres- 
sure exerted, the more luminous it appears. The most marked le- 
sions occur in the proventriculus and are characterized by hem- 
orrhages and erosions in the mucosa. Inflammation is also present 
in the upper portions of the intestines. EcchjTnoses may be pres- 
ent on the heart and in various organs. In cases of long standing 
there may be fatty degeneration of the liver and other organs, and 
yellow colored liver. 



286 DISEASES OF DOMESTICATED BIEDS 

POTASSIUM CYANIDE 

Lethal dose. 1 to 2 grains. 

Toxic dose. Yio to % grains. 

Experiments. (1) February 20, 1918, 10.15 a. m. Gave fowl a 
2 grain crystal of potassium cyanide per os. Symptoms appeared in 
4 minutes. Fowl had difficulty in maintaining its balance. 
Dropped to the floor. After several minutes it fluttered around the 
cage for about five seconds, went down again, became comatose and 
was dead in 12 minutes after swallowing the cyanide. 

(2) February 20, 10.30 a. m. Gave fowl a 1 grain crystal of 
potassium cyanide per os. Symptoms appeared in 2 minutes. 
Fowl became droopy, stood for several minutes with head dropped 
to floor (limber neck), fell to floor in a comatose state and was dead 
13 minutes after swallowing the cyanide. Did not struggle at any 
time. 

(3) July 8, 1918, 2 p. m. Gave fowl a V2 grain crystal of po- 
tassium cyanide per os. 2.02 p. m. Fowl jumped suddenly strik- 
ing top of cage. Stands very erect. Breathing more rapidly. 
Mouth open. 2.05 p. m. Unsteady on legs. Wings drooped. Dis- 
tressed expression. 2.20 p. m. Fowl lying down. Continues 
breathing through mouth. 3 p. m. Same as above. Fowl can stand 
when forced up. 4 p. m. Fowl has recovered. 

(4) February 28, 10.15 a. m. Gave fowl Vo grain of potassium 
cyanide in gelatin capsule per os. 10.23 a. m. Fowl breathing rap- 
idly through the mouth. 10.25 a. m. Wings drooping. Has at- 
tempted to pass droppings four times, each time a very small amount 
has been passed. 10.45 a. m. Same as above. Getting sleepy. 11 
A. M. Same as above. Sleepy. 12 m. 'No change except that 
breathing is not as rapid. 1.30 p. m. Fowl has recovered. 

(5) Aug-ust 12, 2.23 p. m. Gave 3 pound fowl Ko grain potas- 
sium cyanide in small piece per os. 2.26 p. m. Breathing rapidly. 
2.30 p. M. Sitting. 3 p. m. Has depressed appearance. Drowsy. 
Half sitting posture on being placed on feet. Sits again. Breath- 
ing not so rapid. 3.45 p. m. Standing. Some droopiness appar- 
ent. Breathing is normal and fowl is recovering. 4.30 p. m. Ap- 
parently normal. August 13, 9 a. m. Fowl is apparently normal. 

POTASSIUM PERMANGANATE 

Lethal dose. 30 grains. 
Toxic dose. 30 g-rains. 



TOXICOLOGY 287 

ITon-toxic dose. 15 grains. 

15 " in solution, 

1-500 solution as drinking water. 

Experiments. (1) June 25, 1918, 10 a. m. Gave fowl 30 grains 
of potassium permanganate. 4.30 p. m. 'No symptoms noticed. 
June 26, 9 a. m. Fowl died during night. Autopsy notes. Crop 
filled with oats and some water. Dependent portion of crop charred 
and softened. Apparently the mucous membrane was eaten through. 
Submucosa blackened, also skin on lower surface of crop and ad- 
jacent breast. Thick coating of moist black material on lower 
mucosa of crop. Probably remains of permanganate. Several blood 
clots in crop. Remainder of crop mucosa normal. All other organs 
normal. Permanganate had not left crop as far as could be deter- 
mined. Apparently hemorrhage had occurred in subcutaneous tissue 
and blood had been oxidized. 

(2) February 2, 1918, 10 a. m. Gave fowl 15 grains of potas- 
sium permanganate in solution (30 c.c. of dVs per cent solution). 
Result. No effect was apparent. 

(3) July 8, 2 p. M. Gave fowl 15 grains of potassium permanga- 
nate. Result. No effect was apparent. 

(4) June 10, 10 a. m. Gave fowl a 1-500 solution of potassium 
permanganate as drinking water. Fowl drank solution freely. July 
1. Fowl drank about 3000 c.c. of above solution in 21 days. No 
other water was given. Result. No effect was apparent. 

EOSE CHAFERS 

Lamson has observed poisoning of chickens due to eating rose 
chafers {Macrodatylus subspinosus) . 

When opportunity affords, chickens eat rose chafers ravenously. 
Within an hour after feeding the birds assume a dozing attitude. 
Later, weakness is apparent and death usually occurs within 24 hours. 
Convulsions occur in less than five per cent of the cases. 

At autopsy the crop is usually found to be so full of insects as to 
give the impression that death has been due to " crop bound " but no 
abnormal condition of other organs is observed. 

Feeding experiments have shown that 15 to 20 rose chafers are 
sufficient to kill a chicken one week old. From 25 to 45 are neces- 
sary to kill a three weeks old chicken. Ten weeks about marks the 
age limit of susceptibility. The damage is not merely mechanical, 
for an extract of crushed rose chafers in distilled water, after filter- 



288 DISEASES OF DOMESTICATED BIEDS 

ing, will cause death when fed to chickens. The rose chafers ap- 
parently contain a toxin affecting the heart. 

Preventive measures should consist in keeping chickens on mowed 
fields and away from grape vines and flowering shrubs during the 
month when rose chafers are prevalent. 



SALICYLIC ACID 

Lethal dose. 30 to Y5 grains. 

Toxic dose. 30 grains. 

ISTon-toxic dose. 15 grains. 

Experiments. (1) June 10, 1918, 10 a. m. Gave fowl 75 grains 
of salicylic acid. 11.30 a. m. Wings dropped. Fowl sleepy. 
Droopy. 12 m. Condition growing worse. 1.30 p. m. Bird dead. 
Autopsy notes. Crop filled with oats. N"o trace of the three gela- 
tin capsules. At least half of the salicylic acid administered re- 
mains in the esophagus. Mucous membrane of mouth, esophagus, 
crop and lower esophagus is white from action of the salicylic acid. 
Protoplasm is apparently coagulated. IS^ot so severe in lower esopha- 
gus and crop as in upper esophagus and mouth. 'No other lesions ap- 
parent. 

(2) June 25, 1918, 10 a. m. Gave fowl 30 grains of salicylic 
acid. 4 p. M. Fowl droopy. June 26, 9 a. m. Fowl lying on side 
in comatose condition. 2.30 p. m. Fowl died. Autopsy notes. 
Crop filled with food and some white material probably salicylic acid. 
Dependent portion of wall of crop thickened, wrinkled and coagulated, 
white in color. Mucosa of lower esophagus and proventriculus 
whitened. Intestine mildly hemorrhagic throughout its length. Wall 
congested. Liver dark, capsule thickened in one place. Spleen soft. 
Ovary shows B. pullorum infection. 

(3) July 8, 2 p. M. Gave fowl 15 grains of salicylic acid. Re- 
sult. No effect was apparent. 

SANTONIN 

ISTon-toxic dose. 5 to 15 grains. 

Experiments. (1) June 25, 10 a. m. Gave fowl 15 grains of 
santonin. Result. No effect was apparent. 

(2) June 10, 10 a. m. Gave fowl 5 grains of santonin. Result. 
No effect was apparent. 



TOXICOLOGY 289 

SODIUM CHLOEIDE ( COMMON SALt) 

Lethal dose. 2/4 drams. 

2^ drams in solution. 

Toxic dose. Same as lethal. 

N'on-toxic dose. 1/4 to 1% drams. 

Experiments. (1) February 2, 10 a. m. Gave fowl 2^4 drams 
of sodium chloride in solution (40 c.c. of 25 per cent solution). 11 
A. M. Fowl is dull. 12 M. Same. 2 p. m. Same. Droopy. 
Sleepy. 4.30 p. m. Fowl is sitting. Sleepy. February 3, 9 a. m. 
Fowl found dead. Autopsy notes. Considerable food in crop and 
gizzard. Crop, proventriculus and gizzard are normal. Small in- 
testine normal. Rectum slightly inflamed. Liver darkened. Kid- 
ney congested. Heart is systole. 

(2) June 25, 10 a. m. Gave fowl 2^2 drams of sodium chloride. 
June 26, 9 a. m. Fowl droopy. 1 p. m. Paralyzed. 4 p. m. 
Paralyzed. Shows condition known as wry neck. June 27, 9 a. m. 
Paralyzed. Lying on side. Wry neck. 11a. m. Died. Autopsy 
notes. Crop gorged with food. Mucosa of crop white, cooked ap- 
pearance, thickened. Severe catarrh of proventriculus, tenacious 
mucous exudate. Horny membrane of gizzard easily removed. 
Duodenum shows slight congestion. Catarrh of duodenum. Liver 
darkened. 

(3) July 8, 2 p. M. Gave fowl 1% drams of sodium chloride. 
Result. 'No effect was apparent. 

(4) February 28, 10 a. m. Gave fowl iVi drams of sodium chlor- 
ide. 10.30 A. M. Fowl shows a moderate thirst. Result. No ef- 
fect was apparent. 

Suffran observes that fatal poisoning is induced in the hen by a 
dose of 4 grams of common salt per kilo of body weight, while the 
pigeon succumbs to 5 grams per bird. 

The clinical picture of intoxication by salt gives the impression 
that it acts as a poison of the muscles. The gradual weakening of 
the contractile power induces progressive difficulty in walking and 
at last falling down. It is not a true paralysis for sensation and 
movement continue until death. Pricking, and the point of a 
thermo cautery produce response by contraction. The weakening 
of the muscles of respiration causes a progressive asphyxia which 
leads to death. 

The toxic action of salt is exercised also in a certain measure on 



290 DISEASES OF DOMESTICATED BIRDS 

the nervous centers. A proof of that influence is seen in the phenom- 
ena of somnolence which dominate the morbid scene, in the hyper- 
esthesia which is manifested by the transitory crises and last by the 
interference with locomotion. 

The lesions are chiefly in the digestive canal. The buccal mucosa 
is covered with a yellowish brown layer which is viscid and adherent. 
When this is removed, marked congestion is seen, with hemorrhages 
at some points. The mucosa of the crop shows traces of a violent 
irritation with numerous hemorrhages and superficial ulceration. 
The mucosa of the esophagus shows general congestion with super- 
ficial erosions. The intestinal mucosa is hyperemic, hemorrhagic 
and ulcerated. The principal visceral organs such as liver, spleen, 
kidneys, lungs, heart and nervous centers such as brain and cord 
show more or less marked congestive lesions. The blood possesses 
a characteristic bright red color. 

Edwards found that doses of salt as high as 2.5 grams per kilo- 
gram of body weight administered to pigeons by injecting into the 
crop, produced no etfect. A dose of 4.5 grams per kilogram of body 
weight caused great depression, followed by death in eighteen hours. 
A similar dose of 3,3-3 gTams per kilogram caused death in twenty- 
three hours. 'No lesions other than acute congestion of the mucous 
membrane of the lower portion of the esophagus were observed. 
Only about 25 per cent of the salt was absorbed from the crop. 

SODIUM NITKATE 

Lethal dose. 2^/^ drams. 

Toxic dose. 1/4 drams. 

ISTon-toxic dose, /o dram. 

Experiments. (1) February 20, 9.50 a. m. Gave fowl 2% 
drams of sodium nitrate. 11a. m. Fowl dull and droopy, 12 m. 
Fowl shows increased dullness, droopiness and sleepiness. Sitting. 
1 p. M. Fowl is wide awake but dull. Is in a sitting posture. Legs 
paralyzed, cannot stand. 3 p. m. Fowl lying on its side, cannot 
move, legs paralyzed. Greatly depressed. Death appears imminent. 
4.30 p. M. No change from above. February 21, 9 a, m. Fowl 
died during night. Autopsy notes. Crop wall and skin covering it 
dehydrated. These membranes were transparent, dry and tough, 
Proventriculus shows marked catarrhal exudate. Inner membrane 
of gizzard separated from submucosa. Considerable fluid beneath 
inner membrane. Catarrhal enteritis. Duodenal mucosa congested 



TOXICOLOGY 291 

somewhat. Liver dark. Spleen pale. Pancreas enlarged and in- 
filtrated. Heart is systole. Considerable food in crop. 

(2) February 28, 1918, 10 a. m. Gave fowl 1/4 drams of sodium 
nitrate. 1.30 p. m. No change is apparent. 3.30 r. m. Fowl 
bunched up and sleeping. On being aroused displays marked thirst. 
Becomes droopy and sleepy again. 4.30 p. m. Fowl droopy and 
shows thirst. March 1, 9 a. m. Fowl quiet. Sits down. Comb 
and wattles dark red. 12 m. Same as above. 1.30 p. m. Fowl 
paralyzed, no use of feet, prostrated. 3.30 p. m. Same as above. 
Comb blackening at the tips. 4.30 p. m. Same as above. March 
2, 9 A. M. Fowl up, normal in appearance but quiet on being 
handled. Comb a bright red. 3 p. m. Fowl apparently normal. 

(3) June 25, 10 a. m. Gave fowl Yi dram of sodium nitrate. Re- 
sult. No effect was apparent. 

STRYCHNINE SULPHATE 

Lethal dose. 2 gi*ains to 3-1/4 pound fowl. 

Toxic dose. 2 to 3 grains to 5 pound fowl. 
1.5 grains to 3 pound fowl. 
8 c.c. F. E. nux vomica = 1.2 grains to 3 pound fowl. 

Non-toxic dose. 2 grains to 5 pound fowl. 

Experiments. (1) August 12, 2.22 p. m. Gave 3^4 pound fowl 
2 grains of strychnine sulphate in gelatin capsule per os. 2.30 p. m. 
Breathing more rapidly. Some unsteadiness of legs. 2.31 p. m. 
Convulsion lasting 10 seconds. Fowl down on side. 2.32 p. :si. 
Slight convulsion. Rapid breathing. 2.35 p. m. Slight convul- 
sion. 2.36 p. M. Fowl stretched out at length. Rapid shivering of 
legs. 2.40 p. M. Fowl dead. Autopsy notes. Fowl stiff. Con- 
siderable fluid in crop. Heart in systole. Liver slightly congested. 
Comb, wattles and face darkened. 

(2) August 12, 2.23 p. m. Gave 5 pound fowl 3 grains of strych- 
nine sulphate in gelatin capsule per os. 2.45 p. m. Breathing 
rapidly. Unsteady on legs. 2.50 p. m. Sitting. 2.55 p. m. 
Standing. Breathing 180 per minute. 3.45 p. m. Breathing con- 
siderably decreased. Some unsteadiness on legs through lack of 
normal powers of balance. 4.30 p. m. Appears improved. August 
13, 9 A. M. Fowl's legs straddled. Cannot stand up. When dis- 
turbed clonic spasms lasting 4 or 5 seconds are set up. August 14, 
9 A. M. Fowl paralyzed. August 15, 9 a. m. Fowl stands fairly 
erect for a short time but is unsteady on its feet. Diarrhea present. 



292 DISEASES OF DOMESTICATED BIEDS 

August IG. Fowl stands but is unsteady on feet. Mucli improved. 
August 17, 9 A. M. Fowl appears normal. 

(3) July 8, 1.55 p. m. Gave 5 pound fowl 2 grains of strychnine 
in gelatin capsule per os. 2.10 p. m. Fowl unsteady on feet. 2.15 
p. M. Sways over backwards. Weak in legs. 4 p. isr. No other 
change observed. Fowl apparently normal. 

(4) February 19, 2.10 p. m. Gave fowl 1.5 grains of strychnine 
sulphate in gelatin capsule per os. 2.30 p. m. Fowl suddenly af- 
fected. Delay due to slowness of liquefaction of the capsule. Fowl 
staggers, legs spread, bird drops on her side. Several severe spasms 
in first 5 minutes, breathing rapidly. 2.40 p. m. Fowl sleepy, dozes 
for a moment and then starts suddenly, breathing rapidly, no spasms. 
3 p. M. Breathing less labored, fowl still prostrated. 4 p. m. Bird 
in sitting position. Can rise slightly from the floor but cannot stand 
erect. Breathing normal and fowl appears bright and normal other 
than the leg weakness. February 20, 9 a. m. Fowl is apparently 
normal except for incoordination of movement. Unsteady on its feet 
and lifts them higher than normal in walking. February 21. Fowl 
improving in ability to control legs but still unsteady. February 23. 
Fowl apparently normal. 

(5) February 8, 10.30 a. m. Gave fowl 8 c.c. of fluid extract of 
nux vomica (1 per cent strychnine) with 8 c.c. HoO by tube into 
crop = 1.2 grains of strychnine. 10.35 a. m. Fowl nervous. 
Breathing very rapidly. 10.40 a. m. Fowl wabbles^ difficult to 
maintain balance, legs weak, bird does not stand erect. Severe spasm 
of muscles of body and wings lasting 10 seconds. 10.50 a. m. Fowl 
in sitting position from leg weakness or partial paralysis, breathing 
rapidly. Has had three violent convulsions. Comb and wattles red- 
der than normal. 11 a. m. Breathing much slower. No more 
spasms. Bird is recovering. 11.30 a. m. Fowl can stand. 12 m. 
Fowl appears normal. 4.30 p. m. Fowl normal. 

(6) June 25, 10 a. m. Gave 5 pound fowl 2 grains of strych- 
nine in gelatin capsule per os. No effect apparent except a slight 
increase in activity for several moments one hour after administra- 
tion. 

Schneider determined the therapeutic and lethal doses for strych- 
nine nitrate for various birds. His results presented in tabular form 
below refer to doses in milligrams per kilo of body weight. 





1 


rOXICOLOG^ 


Y 




29^ 




Subcuti 


^neous 


Internal 


per 


OS. 




Therapeutic 


Lethal 


Therapeutic 




Lethal 


Geese 


A 


1.0-2.0 


.G 




2.5 


Ducks 


.5-.6 


1.0-1.1 


1.5-2.0 




3.0- 4.5 


Hens 


1.0 


3.0-5.0 


2.0-3.0 




30.0-140.0 


Pigeons 


.5-.75 


1.0-1.5 


6.0 




8.5- 11.0 



It will be observed that pigeons arc least susceptible to internal 
therapeutic doses, while hens, ducks and geese are more so. How- 
ever, with reference to lethal doses per os, hens are most resistant, 
and pigeons, ducks and geese less so. 

The therapeutic doses expressed above in milligrams per kilo of 
body weight, are given below on a basis of milligrams per bird. 

Therapeutic doses 





Subcutaneous 


Per OS. 


Geese 


1.4 


2.16-2.22 


Ducks 


.7 - .96 


2.5 -3.8 


Hens 


.7 -1.5 


2.0 -5.0 


Pigeons 


.16- .26 

SULPHUR 


2.0 -2.4 



IsTon-toxic dose. /4 ounce -f" 

Experiment. (1) February 20, 9.45 a. m. Fowl received M, 
ounce of sulphur. Result. ISTo effect was apparent. Fowl re- 
mained as active as it was previous to administration of the sulphur. 



TARTAR EMETIC 

Lethal dose. 10 to 15 grains. 

Toxic dose. 10 grains. 

]^on-toxic dose. 5 grains. 

Experiments. (1) February 20, 9.40 a. m. Gave fowl 15 grains 
of tartar emetic. 12 m. ISTo special change except that the bird is 
quieter than normal, 1 p. m. Bird quieter than normal. Sits down 
a good deal. 4.30 p. m. Quiet but shows no special symptoms, 
February 21, 9 a, m. Fowl died during the night. Autopsy notes. 
Comb normal. Heart in systole. Crop contains considerable food. 
Proventriculus shows catarrhal condition. Intestine catarrhal. 
Duodenum petechiated. Heart petechiated. Liver pale. Kidneys 
congested. 

(2) June 25, 10 a. yi. Gave fowl 10 gTains tartar emetic. June 
26. j^o apparent change. June 27. ISTo apparent change, June 



294 DISEASES OF DOMESTICATED BIEDS 

28, 9 a. m. Fowl dead. Autopsy notes. Considerable food in crop. 
Mucosa of dependent portion of crop shows a number of small necrotic 
patches and erosions. Mucosa of duodenum hemorrhagic. Liver 
congested and pale in spots. Heart in systole. 

(3) February 28, 10.15 a. m. Fowl received 5 grains of tartar 
emetic. Result. JSTo effect was apparent. 

TURPENTINE 

ISTon-toxic dose. 2% drams + 

Experiment. (1) February 7, 10.30 a. m. Fowl received 2^^ 
drams of turpentine with 2^ drams of linseed oil. Result. 'No ef- 
fect was apparent. 

REFERENCES 

1. Edwards. Salt poisoning in pigs and poultry. Jour. Compar. Path, 
and Ther. Vol. 31, 1918, p. 40. 

2. Gallagher. Experiments in avian toxicology. J. Am. Vet. Med. Ass., 
Vol. 7, 1919, p. 337. 

3. Lamson. The poisonous effects of the rose chafer upon chickens. 
Science, n. s. Vol. 43, 1916, p. 138. 

4. Reinhardt. Beitrage zur Kenntniss der Gefliigelkrankheiten. Berl. 
tierdrztl. Wchnschr., Bd. 30, 1914, S. 214. 

5. Schneider. Toxikologische Versuche mit Strychninum nitricum bei 
Gansen, Enten, Hiihnern und Tauben. Monatschr. f. praM. tierh., Bd. 11, 
1899-1900, S. 245. 

6. Suffran. Sur I'empoisonnement des volailles par le sel de cuisine. 
Rev. Gen. Med. Vet., T. 13, 1909, p. 698. 



CHAPTEK XXIII 

SURGICAL DISEASES 
ANESTHETIZING FOWLS 

Occasions demanding the administration of a general anesthetic 
are limited largely to serious operations undertaken in connection 
with the study of the functions of certain organs. Pearl and Surface 
have pointed out that hy the ordinary method of administration of an 
anesthetic, ninety per cent of the subjects will die under the anes- 
thetic. If less of the drug is administered, reflex excitability is not 
lost, and the bird will struggle. It is likely that the explanation of 
the high mortality lies in the fact that the air sac system of birds 
furnishes opportunity for the storage of a large amount of anesthetic 
which is wholly absorbed in a short time and not eliminated by ex- 
piration as in mammals. The excessive amount of anesthetic prob- 
ably affects the vagus center which causes cardiac inhibition, respira- 
tory failure and death. 

These writers obviate fatal results in anesthetizing hens by inject- 
ing subcutaneously in the axilla 1-200 grain of atropine sulphate dis- 
solved in 1 c.c. of warm normal salt solution. Administration of 
ether follows immediately and the bird will be ready for operation 
in fifteen to twenty minutes. 

ARTHRITIS IN PIGEONS 

Arthritis of the wing joints of pigeons, preventing flight, may be 
caused by a number of infectious diseases such as tuberculosis or 
diphtheria ; by gout or by mechanical injury. Klee observes that 
carrier pigeons are subject to the disease under such circumstances 
as to indicate the existence of a common cause. In affected birds 
one wing usually droops, for involvement of both wings is rare. 
On examination the shoulder and elbow joints will be found to be 
somewhat swollen, reddened and painful. In undertaking treat- 
ment, isolation of the bird is absolutely necessary to ensure rest for 
the joints. He recommends applying a woolen bandage to the wing 
in such a way as to secure immobility and applying lead water to the 
same at frequent intervals. The bandage should be changed every 

295 



S 



296 



DISEASES OF DOMESTICATED BIKDS 



two days. When heat and swelling disappear after 8 to 14 days, the 
bandage is removed permanently and the bird is still confined in a 
cage. The joints may then be painted with tincture of iodine. 
Cases that do not recover in three weeks may be regarded as hope- 
less. When caseous masses form in the joints and neighboring tis- 
sues they may be removed by operation. Birds thus operated upon 
seldom fly again and their future usefulness is limited to breeding. 

BUMBLEFOOT 

Bumblefoot is a suppurative condition of the feet of walking 
birds. It consists of an inflammatoi'y condition involving the burste, 




Fig. 55. Bumblefoot. 



tendon sheaths^ and tendons of the foot. It is reputed to occur most 
often in the heavy breeds and in cocks more often than in hens. 

The diseased feet are swollen and hot to the touch. In extreme 
cases the swelling becomes so large as to interfere with locomotion. 



SURGICAL DISEASES 



297 



In some cases fluctuation occurs and in others the tumor remains 
hard. 

Surgical treatment involves incising the bottom of the swelling to 
allow the escape of the grayish semi-fluid contents. Sometimes the 
swelling contains a caseous mass of a lamellated structure. 

The cavity may be packed with gauze wet with perchloride of iron 
as a hemostatic and the whole foot bandaged. The bird is confined 
to an area not provided with a perch. The wound may be dressed 
every few days, some disinfectant being substituted for the per- 
chloride of iron. Likely the wound will continue to slough, and dis- 
charge an ill smelling secretion. In this event the foot may be bathed 
in a warm solution of compound solution of cresol. Iodine, zinc chlo- 
ride or lunar caustic may be applied to the interior of the wound. 
Often treatment may require months, and necessitate trouble out of 
proportion to the value of the bird. 

Bumblefoot has been attributed to injury resulting from jumping 
from high perches or to roosting on perches of an unsuitable, angular 
character. 



CUTANEOUS EMPHYSEMA 

Emphysema of the skin designates a condition in which there 
is an abnomial amount of air in the subcutaneous region. The 

cause is either a wound or 
spontaneous rupture of the or- 
gans containing air, such as 
the trachea, or the various air 
sacs and passages communicat- 
ing between them. The air 
imprisoned beneath the skin 
may so distend the skin that 
the bird appears almost like a 
ball. 

The condition occurs in 
young canary birds and has 
been reported in fowls, turkeys 
and pigeons. 

Radical correction of the trouble by preventing the leakage is not 
possible, but relief of the condition may be accomplished by slitting 
the skin to prevent accumulation of air. 




Fig. 



56. A young canary bird with em- 
physema of the skin. (Klee) 



298 DISEASES OF DOMESTICATED BIKDS 

CUTANEOUS HOENY GROWTHS 

Horny growths on the skin of birds are not rare. They result from 
a proliferation of the epithelial cells and subsequent hardening of the 
tissue causing deformity. The growths have no effect upon the 
general health. When the location interferes with function as on 
the beak, operative treatment is indicated. 

In parrots cutaneous horny growths occur, which are of tuberculous 
origin. Klee reports that skin horns occur in about 50 per cent of 
parrots affected with tuberculosis. 

DUBBING OR CROPPING 

The removal of the comb and wattles is commonly practiced in pre- 
paring game birds for the ring. It is also performed upon male 
breeding birds of some breeds where the comb and wattles are abnor- 
mally developed. The removal of these structures is said to improve 
the condition of the bird and increase the percentage of fertile eggs. 
The operation is indicated in bad cases of frost bite and in the in- 
fectious disease known as edema of the wattles. 

In removing the comb, the bird is held by an assistant who grasps 
the two legs with one hand and the wings with the other. The 
operator grasps the comb finnly and cuts with a knife from the base 
forward to the beak as close to the head as possible. Hemorrhage 
may usually be controlled by pouring cold water upon the head, but 
if not, the actual cautery may be applied. Curved surgical scissors 
may be employed in removing the wattles, which operation does not 
cause such severe hemorrhage. Antiseptic dusting powders may be 
applied to the wounds. The bird should be kept secluded until the 
wounds have entirely healed, before being turned loose among other 
birds. 

FRACTURED BONES 

Broken bones are not rare among fowls as a result of accidents, 
fighting and mistreatment. Pigeons frequently break wing bones by 
colliding with objects during flight. Bones of the feet may be frac- 
tured when the bird becomes entangled and struggles while hanging 
by the feet. 

A cure is possible and probable if the break is fresh and uncom- 
plicated by splinters, if the soft tissues are not lacerated and if the 
skin is not punctured. Cure is most probable in simple fractures 



SURGICAL DISEASES 299 

of the bones of the leg and feet. The bird is laid upon the back and 
the feathers are clipped from the region of the break. The skin is 
cleaned of blood by washing with three per cent solution of com- 
pound solution of cresol. The two broken ends are brought into the 
correct position. A strip of adhesive tape of the proper dimension 
is wrapped about the broken bone so that there is formed an en- 
veloping band. Care should be taken not to draw the tape too tight. 
Pigeons and most sorts of hens do not require a special splint, for 
the adhesive tape is stiff enough. In the case of very heavy boned 
fowls, ducks and geese it is preferable to use thin strips of wood or 
an envelope of stiff paper as a foundation for the bandage. Goose 
quills, softened in hot water and split from end to end, are useful as 
splints. In the case of weak bones, one quill is enough, but larger 
ones need two quills, one on each side. The softened quill fits itself 
to the bone and is held in place by a bandage. These quill splints are 
at the same time light and strong and consequently are decidedly 
preferable to other material. 

Fractures of wing bones of pigeons are mostly followed by an im- 
pairment of the ability to fly so that treatment is only indicated in 
valuable individuals which can be utilized as breeders. An adhesive 
tape bandage is applied after removal of the feathers as in the case 
of a fracture of a leg bone, only it is useful to make the bandage 
broader and longer. As soon as the bandage is applied, but while 
yet soft, it is pressed with the fingers into a fiat shape correspond- 
ing to that of the wing. The bird is then wrapped with bandages so 
that both wings lie close to the body and the use of even the sound 
one is impossible. 

The bandages are kept in place for about two weeks and in that 
time healing has mostly taken place. To hasten recovery the bird 
is isolated in a cage without perches or in a crate with planer shav- 
ings. In such cases when a bird is confined for a long time, the 
feathers and cage should be thoroughly dusted with insect powder. 
The torments suffered by such a bird from blood sucking insects are 
severe and the restlessness ensuing, retards recovery. 

After removal of the bandages, the bird is to be kept isolated for a 
time from others of his kind for fear that the bone will be broken 
again. 

Swelling of the extremity after bandaging a broken bone indicates 
that the bandage is too tight and that it must be replaced by a better 
fitting one. Often in this case it is too late, and it is better to kill 



300 DISEASES OF DOMESTICATED BIKDS 

the patient because in birds dry gangrene occurs very quickly in parts 
from which the circulation is cut off. (Klee.) 

FEOZEN COMB AND WATTLES 

\\lien freezing of the appendages of the head occurs, thawing may 
be accomplished by smearing with vaseline, and manipulating with 
the fingers. In case of serious injury of the comb or wattles, they 
may be removed as described under dubbing. 

INCISIO^Sr OF THE CKOP 

This operation is frequently necessary in order to evacuate the 
contents of the organ when impaction is present, and is comparatively 
harmless in fowls. After removing the feathers from the operative 
area, an incision is made parallel to the axis of the neck, and as 
long as the circumstances require. The material is removed by 
kneading, and the use of forceps. Healing occurs in about a week 
after suturing. Feeding must be restricted for a few days to bread 
and milk but water may be given without limit after 36 hours. 

PEEVENTION OF FLIGHT 

It is sometimes necessary to deprive birds of the power of flight 
either temporarily or permanently. To arrive at this result it may 
be necessary only to cut off the large feathers on one wing, or to pre- 
vent the extension of the member by some mechanical device. What- 
ever the method employed it should be applied to but one wing. The 
effect in preventing flight is accomplished more by destroying power 
■of maintaining equilibrium than in reducing wing surface. 

Permanent elimination of the primary wing feathers may be ac- 
complished by severing the region of the wing corresponding to the 
hand. A cut is made with scissors on a line so as barely to leave 
intact the bone corresponding to the thumb. The proper location for 
the amputation may be determined by making the cut barely include 
the primary feathers. Hemorrhage may be arrested by cauterizing 
or by applying perchloride of iron. 

The operation is very simple and quite harmless. Very little 
trace is left, for the stump is covered by the feathers of the thumb. 
When the wing is folded, the absence of the primary feathers is not 
noticeable. 



SURGICAL DISEASES 301 



WOUNDS 

Fowls arc liable to be wounded by fighting, by bites of dogs, by 
birds of prey, etc. Treatment consists of clipping off the feathers 
in the vicinity to expose the wounded area. The wound may be 
washed in a three per cent solution of compound solution of cresol. 
TIemorrhago may be controlled by the application of perchloride of 
iron with a pledget of cotton. Slight hemorrhage may be treated 
with styptic collodion. Since the blood of birds, especially of pigeons, 
clots very readily, hemorrhage is usually controlled without difficulty. 
Extensive wounds of the skin may be sutured. Tattered portions of 
muscle may be clipped off smooth with scissors. 

Treatment is more difficult if the wound includes a tear of the 
crop. In such a case the organ must be first emptied of its food 
contents by flushing out with fluid introduced by means of a rubber 
tube. Treatment then is carried out in the same manner as in 
closing an incision of the crop. 

In general, wounds of birds, except the most severe ones, heal 
readily. Suppuration of wounds as in mammals, does not occur in 
birds. 

REFERENCES 

1. Klee. Die hauptsachlichsten Gefliigel-Ivrankheiten. Leipzig. 1905. 

2. Megnin. Medecine des oiseaux. Vincennes : Au Bureaux de 1'- 
Eleven. 1906. 

3. Pearl and Surface. The use of atropine sulphate in anesthetizing 
birds for surgical experiments. J. Am. M. Ass., Vol. 52, 1909, p. 382. 



S 



CHAPTER XXIV 

CAPONIZING 



CAPONIZING THE FOWL 



The operation of caponizing or castration of the male fowl is de- 
scribed by Slocum as follows : 



TIME TO CAPONIZE 



In so far as the effects of the operation and the rapidity and ease 
of healing are concerned, the time of year when the operation is per- 
formed is of little importance. The capons seem to recover and do 
well at any time. Certain other considerations, however, do influ- 




FiG. 57. Barred Plymouth Rock cockerel of suitable size to caponize. 
from photograph by Slocum) 



( Drawn 



ence the time. The age and size of the cockerel are very important. 
As soon as the cockerels weigh 1^2 to 2/^ pounds, or when 2 to 4 
months old, they should be operated upon. The lower age and weight 



302 



CAPONIZING 303 

limits apply particularly to the American breeds, while the higher 
apply to the Asiatics. If smaller than this, their bodies do not give 
room enough to work handily. On the other hand, they should never 
be over 6 months old, as by this time the testicles have developed 
to a considerable extent, the spermatic arteries carry greater amounts 
of blood, and the danger of pricking these arteries and causing the 
fowl to bleed to death is greatly increased. The fact that capons 
are in greatest demand and bring the best prices from the Christmas 
season until the end of March, and that it takes about 10 months to 
grow and finish them properly, makes it important to hatch the 
chicks in early spring so that they will be of proper size for caponiz- 
ing in June, July, and August. These are by far the most popular 
months for the operation, though in some cases it is performed still 
later. 

CAPONIZING INSTRUMENTS 

There are several sets of instruments for performing the operation. 
These differ principally in the type of instrument used in getting 
hold of and removing the testicle. One type is the cannula (Fig. 58, 
a). This consists of a hollow tube, the lower end of which is com- 
pressed and closed except for two small holes through which to run the 
horse hair or wire comprising the other part of the instrument. 
This type requires two hands to operate. Another type is the twist- 
ing scoop (Fig. 58, h). This is a spoon-like scoop slotted in the center 
and mounted upon a slender rod. It is desig-ned to slip under the 
testicle, allowing the spermatic cord to pass through the slot. By 
twisting the cord is severed. This type has the advantage of requir- 
ing only one hand to operate, but is more liable to produce " slips " 
(see p. 309) than the cannula. A third style of instrument (Fig 58, 
i) is also in the form of a spoon or scoop, but instead of being in one 
piece has two jaws regulated by a slide. The testicle is caught in 
the scoop with the spermatic cord between the jaws, and by tighten- 
ing the jaws and gently moving the instrument the cord is severed and 
the testicle removed. Still another type, not now in common use, is 
the spoon forceps. With this the testicle is simply grasped with the 
forceps and detached by a twisting movement. Here one hand can 
be used also, but the liability of slips is rather greater than with the 
other methods. 

Fig-ure 58, Jc, shows a type of forceps, consisting of two hinged 
arms, one of which terminates in a broad, flat surface, and the other 
in an end of similar shape from which the center has been removed, 



304 



DISEASES OF DOMESTICATED BIRDS 




Fig. 58. Instruments used in caponizing. (Slocum) 



leaving only a narrow rim. These two ends are held closely pressed 
together by means of a rubber band passing across the handles. In 
use, the ends of the forceps are separated, the solid one slipped under 
the testicle and the rim then allowed to settle down over it. The 
cord is thus caught and the testicle can be removed. Careless or too 
rapid use of this instrument is likely to cause slips. Figure 58, I and 
m, shows two additional types of testicle removers. The type shown 
in I has a curved handle which brings the hand out of the line of 
vision, making it easier to see into the body cavity when using the 
instrument. A knife for making the incision into the body cavity is, 
of course, necessary. Almost any sharp-pointed, thin-bladed knife 
will answer the purpose well (see Fig. 58, c). Some sort of spreader 



CAPONIZING 305 

to spring apart the ribs far enough to allow the instruments to be 
inserted into the body must be used. A plain spring spreader, as 
shown in figure 58, d, or a sliding spreader (Fig. 58, e), allowing the 
pressure to be gauged, will answer the purpose. A sharp-pointed 
hook (Fig. 58, /t), for tearing away the thin membranes, and a blunt 
probe, of which figure 58, g, is one type, for pushing aside the intes- 
tines, complete the necessary equipment. A pair of small tweezers 
or nippers (Fig. 58, /) is also useful in removing any foreigTi matter 
from the bodv. 



THE OPERATION OF CAPONIZING 

Before beginning the operation two conditions are absolutely essen- 
tial. If these are not favorable, do not attempt to operate. The 
first of these is that the intestines of the fowl should be completely 
empty, so that they will fall away and expose the testicle to view. 
This can be accomplished by shutting up the fowls and withholding 
all food and water for 24 to 36 hours before the operation. With- 
holding water tends to make the blood thicker and consequently to 
decrease the amount of bleeding. Thirty-six hours is better than 24, 
especially for a beginner. The second condition is a good, strong 
light, so that the organs of the fowl may be clearly and easily dis- 
tinguished. Direct sunlight is best for this, and in consequence it is 
well to operate out of doors on a bright day. Some operators have 
substituted the physician's head reflector and artificial light with 
good success. An ordinary incandescent electric bulb fastened to a 
gooseneck standard and provided with a reflector can be used to good 
advantage when caponizing indoors. It has been suggested that a 
probe consisting of a small electric bulb on the end of a slender rod 
and operated by small dry batteries, so that it can be introduced into 
the body cavity, could be manufactured and used with good success. 

METHODS OF HOLDING THE FOWL 

When ready to operate, catch the bird and pass a noose of strong 
string about the legs. Do the same with both wings close to the 
shoulder joints. To the other end of the strings arc attached weights 
of sufiicicnt size to hold down and stretch out the bird when placed 
upon the head of a barrel or box of convenient height, which is to 
serve as operating tal)lc. These weights are allowed to hang on oppo- 
site sides of the barrel or box (Fig. 59). A table, if so desired, may 



306 DISEASES OF DOMESTICATED BIKDS 

be arranged by boring holes through its top at proper distances from 
each other, allowing the strings to pass through these, and hanging 
the weights underneath. Still other ways of holding the fowl in 
place have been devised, but these are unimportant so long as the 
fowl is held securely stretched out. 

DETAILS OF THE OPERATION 

Having fastened the fowl, be sure that all the instruments are at 
hand. It is also well, though not necessary, to have ready some 
absorbent cotton and a dish of water to which have been added a few 
drops of carbolic acid or some other antiseptic. Having once started, 
carry the operation through as quickly as possible. Moisten and 
remove the feathers from a small area over the last two ribs just in 




Fig. 59. Feathers plucked away to make ready for incision. (Drawn from 

photograph by Slocum) 

front of the thigh (Fig. 59). With the left hand slide the skin 
and flesh down, toward the thigh. Holding it thus, make the incision 
between the last two ribs (Fig. 60), holding the edge of the knife 
away from you as you stand back of the fowl. Lengthen the incision 
in each direction until it is 1 to iH inches long. Now insert the 
spreader into the incision, thus springing the ribs apart, as shown in 
figure 61. The intestines will now be visible, covered by a thin 
membrane called the omentum. Tear apart this membrane with 
the hook, and the upper testicle, yellow or sometimes rather dark 
colored and about the size and shape of an ordinary bean, should 
be visible close up against the backbone. By pushing aside the in- 
testines this can easily be seen, and the lower one also, in a similar 
position on the other side of the backbone. Expert operators usually 
remove both testicles through one incision. This is a desirable prac- 



CAPONIZING 



307 




Fig. 60. The incision made. Before making the cut, the skin over the last two 
ribs is pulled down toward the thigh and held there while the incision is made. 
When the bird is released after the operation, the skin slips back into its 
natural position. The cut in the skin is then not directly over the incision 
in the body, with the result that the wound is closed and protected. (Drawn 
from photograph by Slocum) 




Fig. 61. The spreader in place. Tearing open the membranes. (Drawn from 

photograph by Slocum) 

tice, as it saves time and is not so hard on the bird. Inexperienced 
operators will nsnally find it well to attempt the removal of the 
upper or nearer testicle only and to make a second incision on the 
opposite side of the body for the removal of the other testicle. 

If both testicles are to be removed through the same incision, 
remove the lower first, as the bleeding from the upper might be suffi- 



308 



DISEASES OF DOMESTICATED BIEDS 




Fig. 62. Spreader in place. The testicle can he obt^erved lying between the 
jaws of the spreader. (Drawn from photograph by Slocum) 




Fig. 0.3. Kcmoving the testicle. (Drawn from photograph by Slocum) 

cient to obscure the lower. Each testicle is enveloped in a thin mem- 
brane. This may be and probably is best removed with the testicle, 
thouirh some operators tear it open and remove the testicle only. 

The delicate part of the operation is now at hand, owin^ to the close 
proximity of the spermatic artery, which runs just back of the testicle 
and to which the testicle is in part attached. If this is ruptured the 
fowl will bleed to death. The cannula, threaded with a coarse horse- 



CAPONIZING 309 

hair or fine wire, or one of the other forms of instrument previously 
described, now comes into use. If the cannula is used, allow the hair 
or wire protruding from the end to form a small loop just large 
enough to slip over the testicle. Work this over the testicle, being 
careful to inclose the entire organ. Now tighten up on the free ends 
of the hair or wire being careful not to catch any part of the 
artery. If the spermatic cord does not separate, saw lightly with 




Fig. 64. The spreader removed and the weights taken off the wings. Notice 
how the skin slips back over the incision so as to close it. (Drawn from 
photograph by Slocum) 

the hair or wire. When the testicle is free, remove it from the body. 
The method of removing the testicle is shown in figure 63. If only 
the upper testicle has been removed, turn the bird over and proceed 
in exactly the same manner upon the other side. 

After removing the testicle, if the bleeding is at all profuse it is 
well to remove a portion of the blood by introducing small pieces 
of absorbent cotton into the body by means of the hook or nippers, 
allowing them to become saturated and then removing them. Be sure 
to remove all blood clots, feathers, or foreign matter. After the 
testicles and all foreign matter are removed, take out the spreaders, 
thus allowing the skin to slip back over the incision. 

LOSSES DUE TO CAPONIZING 

Even experts are sure to kill some birds, but the loss is small, 
seldom exceeding 5 per cent where any considerable number are 
caponized, and usually not more than 2 or 3 per cent. With be- 
ginners, of course, the percentage is much larger, but with a little 



*« 



310 DISEASES OF DOMESTICATED BIKDS 

practice and care this is soon overcome. Any fowls whicli may be 
killed in this way are perfectly good to eat and are therefore not 
wasted. 

A great deal of practice is required to become expert enough to 
operate rapidly. Consequently it is quite common in localities where 
many capons are grown to hire experts to do the work. These men 
are able to caponize a fowl every two to five minutes, and charge 
from 3 to 6 cents a fowl for the service. It is most humane for the 
beginner to make his first trials upon dead fowls. 

SLIPS 

Many times, particularly with beginners, while the operation seems 
to be entirely satisfactory, the bird will turn out to be what is known 
as a " slip." A " slip " is neither cockerel nor capon, but is between 
the two, possessing the mischievous disposition and the appearance 
of an ordinary cockerel, but, as a rule, being unable to reproduce. 
This condition is due to the fact that a small piece of the testicle is 
left in the body. This piece often grows to a considerable size. As 
the " slips " possess the same restless disposition as the cockerels, they 
grow and fatten little if any better, while they do not bring as good a 
price in the market as the capons. Consequently it is well to use 
every precaution in order to avoid " slips," as they are unprofitable 
as compared with capons. With the greatest care, however, " slips " 
are more common than are deaths due to the operation. The per- 
centage varies all the way from 50 per cent with beginners down to 
2 or 3 per cent with experts. 

CARE OF FOWLS AFTER THE OPERATION 

Upon being released from the operating table the capons are 
usually put in a closed yard where they can find shelter, food, and 
water and can be kept quiet. 'No roosts are provided, as the less fly- 
ing and jumping they do the sooner will the wound heal. The 
capons seem to be very little inconvenienced by the operation, and 
water and soft feed mixed with sweet skim milk can be given imme- 
diately. Some feeders give this in unlimited quantity, while others 
feed more sparingly for a time. Some growers observe no precau- 
tions whatever, giving the birds their full liberty immediately after 
the operation and allowing them to have any sort of feed. 

For a week or 10 days the newly made capons should be carefully 



CAPONIZING 311 

observed to see whether they become " wind puffed." This is a con- 
dition caused by air gathering under and puffing out the skin near the 
wound. When observed it can be readily relieved by pricking the 
skin with a needle or knife and pressing out the air. In about 10 
days or 2 weeks the incision into the body should be entirely healed, 
and, although no special antiseptic methods are employed in the 
operation, blood poisoning or any other trouble seldom results. 

CAPONIZING THE MALE OSTRICH 

According to Elley, whose description of the operation is given 
below, the best age for castration of the ostrich is from eighteen 
months to two years. The testes are then beginning to develop, are 
easily located, but are not yet so vascular as to occasion any prob- 
able risk of hemorrhage. 

Preparation for operation. " Have the birds brought into 
the pen on the afternoon of the day before it is intended to operate, 
so that they may have no food whatever for say twenty hours before 
the operation, as the less ingesta in the stomach and bowels, the bet- 
ter and easier it will be. If possible there should be three adjoining 
pens; the first in which to catch the birds, the second or middle for 
operating in, and the third in which to place the birds after the opera- 
tion. The operating pen should be well sprayed with a disinfectant 
solution before commencing. The first bird is caught and brought to 
the operating pen and the chloroform bag placed on his head with 
rather less than half an ounce of chloroform (2-3 teaspoonfuls) on 
the cotton wool. One good boy can then hold him until he is properly 
under the influence of the anaesthetic. A little more chloroform can 
be added after he is down, and if necessary once or twice during the 
operation. One ounce, or at the most one-and-a-half ounces, should 
be sufficient for the whole operation. Ascertain by moving the wings 
or striking him, if he is properly under, then place him on his left 
side. A boy now grasps the right leg and brings it slightly further 
forward than at right angles to the body. The seat of the operation 
is now exposed. It lies in the angle formed by the leg and the lower 
edge of the innominate bone, about three inches behind the former 
and one-and-a-half inches below the latter. The innominate bone 
can be felt as a distinct ridge running backwards and slightly down- 
wards, about the middle of the body immediately behind the leg; it 
corresponds to the lowest part of the body on which any feathers 
are found. It is immediately below this ridge that the incision is 



312 DISEASES OF DOMESTICATED BIRDS 

made. The operator should now wash his hands and the seat of the 
operation with a disinfectant solution. 

The operation. Make an incision about four inches long, cut- 
ting from before backwards, in a line parallel with the ridge men- 
tioned above. Cut down until the peritoneum or thin membrane 
covering the bowels is reached. Care is required at this point. 
Having reached the peritoneum grasp it with the forceps, taking care 
not to include any of the gut, and draw it slightly towards the ex- 
ternal wound, then make an opening through it just large enough 
to admit the hand. Pour a little carbolic oil over the right hand and 
force it gently through the opening into the abdominal cavity. The 
testes are easily located about three to four inches further forward 
than the incision, almost exactly between the upper extremities of 
the two legs, situated on and closely attached to the middle of the 
roof of the abdominal cavity, immediately below the kidneys. In 
birds of an age which I have recommended for the operation they 
are felt as two elongated firm structures, about one-and-a-half inches 
long by a quarter of an inch broad, somewhat the shape of a 303 
bullet. They lie about two inches apart, the left usually slightly 
more forward than the right. Having located them, the tissue round 
about them is easily broken down by the fingers, and a few twists 
liberate them and they fall into the palm of the hand. Both testes 
should be located before either is removed. With care the one can 
be liberated and held in the palm of the hand whilst the fingers 
free the other one. It is then only necessary for the hand to enter 
the abdominal cavity once and be once withdrawn, containing both 
testes. If the birds are in very good condition there will be a certain 
amount of fatty tissue round the testes which may give a little 
more trouble in removing them. Having withdrawn them it only 
remains to suture the wound. Thread a needle with fine cat-gut and 
put two or three stitches through the peritoneum or membrane tak- 
ing care not to prick the gut in doing so. Then stitch the external 
wound with three or four stitches including the skin and muscle. 
Dress the external wound with a little iodoform and the operation 
is complete. Whilst the last stitches are being put in, the chloro- 
form bag should have been removed. Allow the bird to lie quietly 
until he wakes up and let him take his own time about rising, on 
no account frighten him up or he will invariably attempt to rise be- 
fore the effects of the chloroform have quite passed off and in fall- 
ing or struggling the stitches may be broken. Watch the breathing 
throughout the operation, it should be steady and regular. Should 



CAPONIZING 313 

it become jerky or irregular, at once open the end of the cliloroform 
bag and admit more air. 

After treatment. For the first twenty-fonr hours after the op- 
eration the birds should be placed in as quiet a camp as possible, 
where they are not likely to be frightened or made to run. Green 
alfalfa is the best food both before and after the operation. 

Instruments. All the instruments required by any one operat- 
ing by this method are: (a) chloroform bag, such as the one I have 
had made, (b) sharp knives, (c) needles and cat-gut, (d) needle 
holder. This latter will be found useful for the deep stitches in the 
peritoneum. 

Advantages resulting from the operation. Having described 
the operation I will briefly enumerate the advantages which it is 
claimed will result from it. 

1. It is claimed that with the increased condition of the bird which 
is sure to follow the operation, there will be increased weight of 
feathers. 

2. That owing to the quieter life of the bird the feathers will 
be less damaged by fighting or scraping on the ground than in the 
entire bird. 

3. In droughts or when food is scarce, castrated birds will keep 
in fair condition where entire birds would starve. 

4. I believe the flesh of a capon will prove an acceptable article 
of human food. I am quite prepared for this idea to be ridiculed 
today, but in time to come it may be considered." 

REFERENCES 

1. Elley. Castration of ostriches. Agr, J. Cape of Good Hope, Vol. 
29, 1906, p. 349. 

2. Slociim. Capons and caponizing. U. S. Dep. Agr. Farmers' Bull. 
8W, 1917. 



CHAPTER XXV 

KILLING POULTRY 

Results of bad bleeding. The manner in which, fowls are 
slaughtered and bled out has an important bearing upon the ap- 
pearance and keeping quality of the product. Poorly bled fowls 
often show red dots where the feathers have been removed, espe- 
cially in areas over the thighs and wings. Also, veins are seen to 
stand out prominently over the breast, angles of the wings, or on 
the neck. In poorly bled birds the neck is the first part to discolor. 
At first it is red, later bluish red or purple and still later, green. 
The bad appearance of poorly bled carcasses detracts from their 
value and their keeping qualities are very much impaired. 

Pennington and Betts have made an anatomical study of the 
blood vessels of the head and neck of the chicken with reference to 
determining the most satisfactory method of securing complete bleed- 
ing. Their description of proper methods of killing, and discussion 
of faulty methods are quoted as follows. 

" CUTTING " TO BLEED AND " STICKING " TO BEAIN 

When the feathers are removed by scalding, the bird is killed by 
bleeding alone, hence the cuts to sever the veins are the only ones 
attempted, and if the attempt fails bad bleeding will surely result. 
If, on the other hand, dry picking is to be practiced, the birds are cut 
to bleed and are also stuck through the brain to paralyze the feather 
muscles. The latter operation is sometimes performed by running 
the knife under the eye at such an angle that its point will touch the 
skull midway between the eyes and a little behind them; or the 
braining is accomplished by placing the knife about halfway down 
the groove in the roof of the chicken's mouth, and then thrusting it 
up until the knife reaches the top of the skull. The knife, as in 
sticking under the eye, should touch the brain in the back part of 
the skull. The point of the knife should then be twisted slightly, so 
that enough brain tissue may be destroyed to paralyze the bird and 
cause the feathers to loosen. If the " outside-stick " method is prac- 
ticed, practically no blood escapes. If, on the other hand, braining 

314 



KILLING POULTRY 



315 



inside of the mouth is adopted, the blood vessels in the brain which 
are cut find an outlet for their contents through the knife hole. 
Bleeding from these vessels is, under any circumstances, of assistance 
in obtaining the best results, and where the neck vessels are missed 
the condition of the chicken is often greatly improved by the bleed- 
ing from the brain. 



DISCUSSION OF THE ILLUSTKATIONS 



LOCATION OF VEINS 

The location of the principal veins in the neck of the chicken, 
their relation to the skull, and the point at which it is desirable 
to make the cut for bleeding, are sho^vn in the accompanying illus- 
trations. Figure 65 shows the head and neck of a young cock about 

a year old. Two large veins (heavily 
lined with black in the figure) run the 
whole length of the neck, one on each side, 
and unite by a " bridge-vein " which is 
just below and behind the ear. This vein, 
which connects the two others, does not 
run straight across but at an angle, so that 
it is farther front on the left than on the 
right side. If the feathers on the neck of 
a chicken are pushed aside, or, better still, 
if a molting chicken with but a few 
feathers is observed, these veins can be, 
seen at each side of the neck while the 
bird is alive, especially if a little pressure 
is used at the lower part of the neck so that 
the blood collects and distends them. It 
is important that the position of these 
veins be exactly located on the neck of the 
live bird, since upon this information will 
depend very largely the proper guiding of 
the knife to the blood vessel. 

Fig, 66 shows two sketches of a chicken's 
head from which the lower jaw has been re- 
moved. The lower jaw of the chicken is 
Fig. 65. External view of much longer than the beak. It runs back 

pSftior'ot "41^.""?^ to. ^ P<>!"> J"^t Mow the ear, where the 
nington and Betts) hinged joint cau be felt. The skin which 




316 



DISEASES OF DOMESTICATED BIEDS 



makes the corner of the mouth and limits the length of the beak ends 
is indicated in the anatomical drawing marked "A." The skin and 
lower jaw have been cut awaj in order that the position of the veins 
which lie far back on the roof of the mouth and just below its surface 
may be seen. The groove which occurs in the roof of the chicken's 
mouth is a guide to the position of the blood vessel which it is desir- 
able to cut, this point being behind and to the left of the end of the 
groove when the chicken is held head down and with the lower side 
of the head uppermost. The direction and position of the cut which 




coffJi£CT ct/r 



GROO\/e /// 



EYE. 
eNO OF BEAK 







Fig. 66. Lower jaw removed, showing position of veins, anatomy of skull, and 
location of cut. (Pennington and Betts) 

is to sever the veins is shown in Fig. 66 to be on the left side of the 
chicken's head when in the position just described. Because the 
short blood vessel connecting the two long veins, which we have 
termed the " bridge," does not run straight but at an angle, the point 
just indicated is farthest front and the most easily reached by the 
knife. As stated before, these veins lie just below the skin of the 
roof of the mouth, hence a deep cut is not needed, neither is any 
amount of strength required for the operation. 

It will be observed that just in front of the line which indicates the 
point at which these veins are to be cut they divide into two small 
branches, the course of which is not further shown. This is because 
they very soon pass through small holes in the bone and go into the 



KILLING POULTKY 317 

inside of the skull, and into the deep tissue, where they are quite 
safe from the killer's knife. If, then, these large veins are to be sev- 
ered, the cut must be made far enough back to reach them before 
they penetrate the bones of the skull. On the other hand, if the cut 
is made too far back and over the edge of the skull, as will be dis- 
cussed in connection with Fig. 6Q, B, much of the blood will settle in 
the loose tissue of the neck instead of running out of the mouth, 
thereby clogging the vessels and preventing complete bleeding, as 
well as making unsightly discolored areas on the neck near the head. 
It is better to make one cut as shown in this plate rather than to 
cut the " bridge " in the middle or to cut each side vein separately, 
since this sometimes results in the clotting of the blood at the ends 
of the veins before the bleeding is completed. 

ANATOMY OF THE SKULL 

From what has been said concerning the necessity of cutting far 
back in order to reach the point desired, it will be seen that it is 
necessary to know something of the position and shape of the bones 
of the chicken's skull and their relation to the external parts of the 
head. This information is given in Fig. 66, B. Dotted lines 
around the drawing of the skull show the position of wattles, comb, 
etc. In this sketch, too, is shown clearly the length of the chicken's 
jaw, as before mentioned. Its hinge will be found on the head of 
the live bird just below the ear. Still farther back there is a 
U-shaped depression in the skull into which fits the upper part of the 
spinal column. The spine is not shown in the sketch, but the bridge 
vein connecting the two large veins of the neck lies directly across the 
U-shaped depression. 

It can be seen by studying this drawing how far back the knife 
must go if the veins are to be cut at the angle, and it will also be ob- 
served that when they are cut in this position the knife will have a 
bony backing which will prevent it from going too deep, thereby 
obviating the spongy mass of blood in the neck tissues which was dis- 
cussed in connection with Fig. 66, A. This illustration also shows 
where the fingers can grasp the head of the chicken firmly and yet 
not press against the soft parts of the neck. Just above the angle of 
the jaw — that is, about at the chicken's ear — there is a smooth, 
strong area of bone large enough to support the thumb on one side 
and the forefinger on the other, and this is where the head should be 
held while killing. 



N 



318 



DISEASES OE DOMESTICATED BIKDS 



POSITION OF HAND AND KNIFE 



Figure 67 shows the position of a chicken ready for killing and 
held by the feet in a U-shaped shackle. Notice that the thumb of 
the killer is pressed finnly down on the head just below and behind 




Fig. 67. Correct grasp of head at angle of jaw and position of small knife when 
cutting vein. (Pennington and Betts) 

the ear in the space to which attention was called when discussing 
the bones of the skull. Here, too, is the hinge of the jaw. Pressure 
of the thumb on one side of this portion of the skull and on the other 
side at the same place with the forefinger, or with the forefinger and 
second finger, will result in opening the chicken's mouth and holding 
it open while the operator makes the cut to bleed. Held in such 
fashion, there is nothing to constrict the blood vessels, thereby pre- 
venting the blood from escaping even though these vessels be cut. 
The pressure against the jaw makes accurate cutting of the veins 
easier, since the bird can not close its mouth until the pressure is 
removed. Of course, care must be taken not to stretch the neck 
unduly, else the vessels will be pulled to such a narrow diameter 
that they are more difficult to find and also more difficult to empty. 
The position of the knife in the mouth, which is shown by the 
dotted line, needs no further explanation. The knife itself, how- 
ever, is very different from that ordinarily used in the bleeding of 



KILLING POULTRY 



319 




Fig. 68. Location of cuts in mouths of badly bled chickens (lower jaw removed). 

(Pennington and Betts) 

chickens. The knife in common use is much too large, both too 
long and too broad for the most successful work. Generally it is 
provided with a heavy handle, large enough to be grasped easily 
by a large, strong hand. As has already been observed in this dis- 
cussion, the heavy slashing inside the bird's mouth is not only fre- 
quently futile so far as cutting the veins goes, but is really harmful 
in that it makes a pathway for the entrance of bacteria and the con- 
sequent hastening of the bird's decomposition. The operation calls 
for accuracy rather than for strength, and therefore it is desirable 
that the knife should have a smaller handle, which can not be gripped 
so hard. The blade of the knife should be about 2 inches long and 
one-fourth of an inch wide and of a heavy piece of steel, so that it 
will not bend. It is advisable, therefore, to have the back of the 
blade about one-sixteenth of an inch thick. It should be made of 
good hard steel and ground to a sharp point with a straight cutting 
edge, the slope for the point being taken from the back rather than 



320 



DISEASES OF DOMESTICATED BIEDS 



from the edge. Tlie working space in the back part of the month of 
the chicken where the blood vessels lie is very small. Often the 
knife which is used by the killer is too broad to go into this space 
without cutting the sides of the mouth, and as for turning and guid- 
ing it, that is quite out of the question. 

EXAMPLES OF BAD CUTTING 

Ineffectual cutting, due to lack of knowledge of the structure of 
the chicken's neck and head, the use of force rather than skill on the 
part of the operator, and a knife ill adapted to the work which it has 
to do, is illustrated in Figs. 68 and 69 which show some of the most 
common types of cuts in badly bled chickens. A study of these illus- 
trations indicates very plainly why these chickens are badly bled. 
The lower jaws from these heads were removed so that the position 
of the cuts could be noted. Head A has had two cuts. One has run 




Fig. 69. 



Attempts at " cross cutting," showing veins untouched. 
and Betts) 



( Pennington 



KILLING POULTKY 321 

parallel with the connection between the two veins and very close to 
it but has not cut it, and another has run from the angle of the 
mouth to close to the point where the blood vessel on the left side 
of the head breaks into the two smaller vessels and penetrates the 
bones of the skull. The only vessels which were cut in this chicken 
were the small superficial veins supplying the roof of the mouth and 
from which the bleeding amounted to almost nothing. Head B 
shows a cut in the right direction but it did not go quite far enough 
back to reach the veins at their junction. Head A, in Fig. 69, shows 
the cross cut which is advocated by so many killers. In this case it 
was made too far front. Both of the large veins escaped and only 
the small vessels of the roof of the mouth were disturbed. " B " 
is a good illustration of indiscriminate cutting by a badly directed 
knife, which in all probability was far too large, since the upper cut 
extends all the way across the roof of the chicken's mouth and almost 
as far front as the beak. Another cut which partly follows the groove 
in the roof of the mouth would indicate that the killer had tried to 
make a cross cut. 

Such examples of bad cutting might be multiplied indefinitely. 
Yet the general principle is the same and the result is the same — 
namely, a fowl which is not completely bled, which is unsightly, even 
in the packing house, and which deteriorates as a food stuff more 
rapidly than does the well-bled chicken under similar conditions. 



SUMMARY 

The facts which have been stated in the foregoing pages may be 
summarized as follows: 

(1) Grasp the chicken when killing by the bony part of the skull. 
Do not let the fingers touch the neck. 

(2) Make a small cut inside the mouth on the left side of the 
throat just where the bones of the skull end, using a narrow-bladed 
sharp-pointed knife. The direction of the knife is upward and to- 
ward the left when the bird is held head downward with the throat 
toward the operator while killing. 

(3) Brain for dry picking by thmsting the knife through the 
groove which runs along the middle line of the roof of the mouth until 
it pierces the brain in the back part of the skull, causing a loosening 
of the feathers. 

(4) For chickens use a knife the blade of which is 2 inches long. 



322 DISEASES OF DOMESTICATED BIEDS 

one-fourth incli wide, with a thin, flat handle, a sharp point, and a 
straight cutting edge. For turkeys the blade may be 2^ inches long. 
Keep knives very sharp. 

REFERENCE 

1. Pennington and Betts. How to kill and bleed market poultry. TJ. 8. 
Dep. Agr. Bureau Chemistry Circ. 61, Revised. 



AUTPIOR INDEX 



Adam and Medler, 254, 259 
Aragao, 141, 144, 203, 206 
Archibald, 229, 240 

B 
Balfour, 118 
Beach, 109, 189 
Beach and Halpin, 118 
Beach, Lother and Halpin, 108, 109 
Belfanti and Ascoli, 86 
Bertegh, 97, 109 
Bevan, 136, 144 
Binder, 252, 254, 260 
Bishopp, 221, 225 
Bishopp and Wood, 208, 209, 210, 211, 

212, 216, 218, 225 
Bordet and Fally, 107, 109 
Borrel, 97 

Boyce and Warrington, 19 
Bradley, 19 
Bugge,"^ 250 
Burnet, 19, 109 
Burnett, 98 

Bushnell and Maurer, 79 
Butterfield, 146 



C 



Cardamatis, 203, 206 

Centanni, 86 

Chauveau, 19 

Ciurea,' 206 

Claussen, 61, 65 

Cobbold, 63 

Cogny, 39 

Colucci, 178 

Cominotti. 82, 86 

Cornil and Toupet, 250 

Curtice, 50, 65, 121, 126, 242, 250 

Curtis, 261, 274 

Cushman, 126 



Danielewski, 203 
Dawson, 50, 64, 143, 144 
Dickson, 154, 177 
Dodd, 140 
Douglas, 229 
Dubois, 86, 143, 144 
Dupuy, 65 

E 

Eastwood and Griffith, 89 

Edwards, 290, 294 

Ehrenreich, 262, 274 

Ehrenreich and Michaelis, 262, 274 

Ehrhardt, 142, 144 

Ellenberger, 19 

Ellenberger and Baum, 19 

Ellerman and Bang, 146, 149 

Elley, 311, 313 



Fantham, 127, 134, 204 

Fiorentini, 46, 47, 48 

Freese, 83, 86, 190, 246, 247, 250, 255 

Friedberger and Frohner, 97 

Frosch and Birnbaum, 243, 250 

Fuller, 225 



G 



Gage and Hyland, 79 

Gage and Martin, 79 

Gage and Opperman, 160, 206 

Gage and Paige, 80 

Gallagher, 16, 39, 48, 109, 163, 276, 294 

Gerlach, 199 

Gilruth, 254, 260 

Gorig, 271, 274 

Gray, 203, 233, 260 

Greve, 31, 33 

Gutberlet, 187, 206 



H 



Dammann and Manegold, 30, 33 



323 



Hadley, 36, 48, 65, 120, 126, 193, 206 
Hadley and Beach, 109 



324 



AUTHOR INDEX 



Haidub, 225 

Halasi, 97, 109 

Faring and Kofoid, 98, 103, 109 

Harrison and Streit, 107, 109 

Hasenkamp and Sachweh, 246, 251 

Hassall, 225 

Hastings and Halpin, 95 

Hauer, 140, 144 

Hausser, 107, 109 

Hebrand and Antoine, 150, 177 

Herms and Beach, 189, 206 

Herrick, 211, 225 

Hertel, 86 

Higgins, 48 

Hindle, 144 

Hutcheon, 238 



Iturbe and Gonzales, 204, 206 

J 

Jackley, 108, 109 
Joest, 86, 254, 260 
Jones, 75, 77, 80, 274 
Jowett, 43, 48, 134, 144, 240 

K 

Kanpp, 19 

Kern, 260 

Kinyoun, 252, 260 

Kionka, 151 

Kitt, 39, 48 

Klee, 177, 189, 197, 295, 298, 300, 301 

Klein, 50, 62, 65 

Kleine and Moellers, 87 

Koch, 263, 265, 274 

Koch and Rabinowitsch, 95 

Kon, Yutaka, 146 

Kraus and Schiffmann, 87 



Lignieres and Petit, 119 

Lignieres and Zabala, 59, 66 

Lipschutz, 87 

Lisi, 42, 249, 251 

Lode and C ruber, 87 

Loer, 18, 19 

Loffler, 243, 246, 251 

Lounsbury, 225 

Lucet, 43," 48, 119, 246, 247, 251 

Mc 

M'Fadyean, 43, 48, 243, 251 

M 

Mack, 109 

Mack and Records, 48, 109 

Maggiora and Valenti, 87 

Magnussen, 28, 33 

Mane, 87 

Manegold, 31 

Manninger, 254, 260 

Manteufel, 109 

Marchoux and Salimbini, 141, 144 

Martel, 61, 66 

Martin and Daille, 194, 206 

Martin and Robertson, 193, 206 

Marx, 231, 232, 233, 240 

Marx and Sticker, 97, 98 

Matruchot and Dassonville, 119 

Mazza, 44, 48 

Megnin, 65, 157, 187, 189, 195, 301 

Meyer and Crocker, 134 

Miessner and Schern, 252, 260 

Milks, 126 

Mohler and Buckley, 119 

Mollhoff, 143, 144 ' 

Moore, 50, 53, 56, 66, 95, 96, 107, 126, 

185, 206 
Morse, 63, 66 
Murphy and Rous, 274 



N" 



Lamson, 287, 294 

Lamson and Manter, 211, 225 

Landsteiner and Berliner, 87 

Lange, 274 

Laurie, 225 

Leclainche, 45, 48, 87 

Leiclitenstern, 54, 65 

Lewin, 272, 274 

Lignieres, 61, 66 



Neumann, 119, 183, 188, 192, 194, 200, 

202, 206, 209, 220, 240 
Nocard and Leclainche, 42, 48 
Noguchi, 135, 145 
Norgaard and Mohler, 28, 33 



Ostertag and Bugge, 87 



AUTHOR INDEX 



325 



Ostertag and Wolfhiigel, 87 
Ottolenghi, 81, 87 
Owen, 19 



Palamidessi, 66 

Pasteur, 39, 48 

Pearl and Surface, 295, 301 

Pearl, Surface and Curtis, 27 

Pennington and Botts, 314, 322 

Pereira, 145 

Petit and German, 274 

Pfaff, 252, 260 

Pfeiler, 254, 260 

Pfeiler and Rehse, 66 

Pfeiler and Roepke, 50, 66 

Pick, 262, 274 

Pickens, 146, 149, 263, 274 



R 



Eabieaux, 42, 49 

Ransom, 179, 183, 195, 202, 206 

Regenbogen, 272, 274 

Reinhardt, 278, 294 

Reinholdt, 60, 66 

Reischauer, 98 

Repp, 216, 225 

Rettger, 80 

Rettger and Harvey, 68, 80 

Rettger, Hull and Sturges, 80 

Rettger, Kirkpatrick and Card, 80 

Rettger, Kirkpatrick and Jones, 80 

Rettger, Kirkpatrick and Stoneburn, 80 

Rettger and Koser, 66 

Rettger and Stoneburn, 80 

Rieck, 252, 260 

Riemer, 243, 251 

Ritzier, 280 

Robertson, 206, 225, 231, 232, 233, 238, 

240, 241 
Rous, 268, 269, 274, 275 
Rous and Lange, 270, 275 
Rous and Murphy, 269, 275 
Rous, Murphy and Tjtler, 267 
Russ, 87 



Sabouraud, 119 

Sabouraud. Suis and Suffran, 119 

Salmon, 27, 220 

Sanfelice, 62, 66 

Schantyr, 161 



Scherago and Benson, 79 
Schlegel, 275 
Schmid, 97 
Schneider, 292, 294 
Seddon, 41, 49 
Sigwart, 97, 107 
Slocum, 302, 313 
Smith, 120, 126, 193, 242 
Smith and Ten Broeck, 66 
Steen, 19 
Stevenson, 190 
Stiles, 206 
Suffran, 289, 294 



Tartakowski, 259, 260 

Taylor, 50, 66 

Theiler, 226, 241 

Theiler and Robertson, 236, 241 

Theobald, 189, 198, 206, 207 

Tretop, 45, 49 

Tytler, 275 

Tyzzer and Ordway, 265, 267, 273, 275 

U 

Uhlenhuth, 140 

Uhlenhuth and Manteufel, 97 



Vages, 39 

Van Es and Schalk, 92, 94, 95 

W 

Walker, 200, 228, 229, 239, 241 
Ward, 34, 36, 49, 95, 280 
Ward and Gallagher, 80 
Warthin, 146, 149, 226, 275 
Wasielewski and Hoffmann, 252, 260 
Watson, 275 
Weil, 40 

Weinzirl, 193, 207 
Wickware, 205, 207 
Wilcox, 200, 207 
Willach, 250, 251 
Williams, 199, 207 

X Y Z 

Yutaka Kon, 146 
Zeiss, 66, 252, 254, 260 



s 



326 AUTHOR INDEX 

Zeiss and Schlegel, 61 Ziirn, 252 

Zingle, 57, 66 Ziirn and Pauly, 272 

Zundel, 199 Zwick, 260 



SUBJECT INDEX 



Abdomen, drooping, 173 

Acanthia columbara, 2] 4 

Acanthia lectularia, 213 

Acetabulum, 4 

Acorn poisoning in the ostrich, 240 

Aggressin for fowl cholera, 40 

Air sacs, 15 

Air sac mite, 198 

Alimentary system, 10 

tract, diseases of, 154 
Aloes, Barbadoes, 240 
Ammonia, 237 
Ammonium chloride, 277 
Amoeba meleagridis, 120, 193 
Amcebotfpnia sphenoides, 183 
Analges bifidus, 220 
Anesthetizing fowls, 295 
Anatomy, 1 
Anise oil, 191 
Anthrax in the fowl, 143 

in the ostrich, 226 

vaccine, 227 
Apoplectiform septicemia, 28 
Areca nut, 187, 190 
Argas americanus, 221 

miniatus, 221 

reflexus, 224 
Arsenious acid, toxicity, 278 
Arteries, 6 

Arthritis in pigeons, 295 
Ascaridia perspicillum, 169, 188 
Ascaris crassa, 188 
Ascites, 173 
Aspergillosis in the fowl, 111 

in the ostrich, 228 
Aspergillus fumigatus. 111, 230 

candidus, 112 

glaucus, 112 

nigressens, 112 
Asthenia of fowls, 64 
Atropine sulphate, 295 
Autopsy directions, 25 
Avian diphtheria. 96 

salmonellosis, 59 

tuberculosis, 88 



B 



Bacillary white diarrhea, 68 



327 



Bacillus avicida, 34 

avisepticus, 34 

bipolaris septicus, 34 

canariensis necrophorus, 253 

cholerse gallinarum, 34 

coscoroba, 45 

enteritidis, 60 

gallinarum, 50 

loxiacida, 259 

paratyphosus B, 57, 58, 60, 252, 254 

septicemia anserum exudativae, 243 

suipestifer, 56 
Bacterium anthracis, 226 

asthenise, 64 

diphtheriae, 108 

pullorum, 52, 68 

pullorum infection in grown fowls, 74 

sanguinarium, 50 

tuberculosis, 88 

typhi gallinarum alcalifaciens, 50 
Balsam of Peru, 220 
Bed bugs, 213 
Bertiella delafondi, 183 
Bichloride of mercury, disinfectant, 23, 
40 

toxicity of, 279 
Bilharziella polonica, 194 
Bird fever, 252 

flea, 212 

pest, 81 

plague, 81 

pox, 96 
Bismuth subnitrate, toxicity, 280 
Blackhead, 120, 193 
Blastomyces anseris, 194 
Blastomycosis, 194 
Blood. 7 

platelets, 8 

spots in eggs, 169 
Blue stone, toxicity, 282 
Bones, broken, 298 
Boracic acid, 105 
Bothriotaenia longicollis, 183 
Brisket, 3 
Bronchitis, 162 
Brooder pneumonia. 111 
Bumblefoot, 296 
Bunodera linearis, 192 
Bursa of Fabricus, 13 

distention of. 161 

parasites of, 194 



328 



SUBJECT INDEX 



Calcium oxide, toxicity, 280 

Calomel, toxicity, 281 

Camphor, powdered, 198 

Canary birds, infectious diseases of, 252 

fever, 252 
Canker, 96 
Caponizing cockerels, 302 

ostrich, 311 
Caraway oil, 219 
Carbolic acid, disinfectant, 23 

toxicity, 281 

vermifuge, 236 
Carcinoma, 262 
Carpal bones, 4 
Caruncle, 18 
Castor oil, toxicity, 282 
Catarrh, 96 

contagious, 96 

of crop, 155 
Catechu, 133, 282 
Ceea, 13 

Cercomonas hepatica, 194 
Cerebellum, 9 
Cestodes, 182 
Chalk, powdered, 198 
Chicken cholera, 34 
Chiggers, 217 
Chigoe. 213 

Chilomastix gallinarum, 193 
Chloride of lime, disinfectant, 23 

toxicity, 282 
Chlorinated lime, 23 
Choanotrenia infundibulum. 183, 184 
Cholera-like septicemias, 42 
Cholera des poules, 34 
Cimex columbara, 214 

inodorus, 214 

lectularia, 213 
Circulatory system, 6 
Clinostomum commutatum, 192 
Cloaca, 13 
Cloacitis, 167 

Cnemiodocoptes mutans, 218, 219 
Coal tar disinfectants, 23 
Coccidiosis, 127 
Coccidium avium, 127 
Colds, 96 

Colibacillosis tetraonidarum, 63 
Collodion, styptic, 301 
Colon bacilli," septicemias caused by, 61 
Comb, 18 

frozen, 300 
Compound solution of cresol, 22 
Congestion of lungs. 162 
Connective tissue, mites in, 202 
Constipation, 160 
Contagious catarrh, 96 



Copperas, toxicity, 283 

Copper sulphate, toxicity, 282 

Coracoid, 3 

Corrosive sublimate, disinfectant, 23 

toxicity, 279 
Coryza, 96 
Coscoroba swans, 45 
Cotugnia diagonopora, 183 
Creosote oil, 23 
Cresol, compound solution, 22 
Crop, anatomy, 10, 12 

catarrh of, 155 

impaction of, 156 

incision of, 300 

inflammation of. in pigeons, 156 

parasites of, 178 
Cropping wattles, 298 
Crude carbolic acid, 23 

petroleum, 216 
Cryptococcus anseris. 194 
Cutaneous emphysema, 297 

horn, 298 
Cvclocnplum arcuatum, 195 

"mutabile, 192 
Cysto-adenoma, 263 
Cytodites nudus. ins 
Cytoleichus nudus, 198 

D 

Daphnia pulex, 181 
Davainea cantaniana. 183 

cesticillus, 183 

crassula. 183 

echinobothrida, 183 

friedbergeri, 183, 184 

proglottina, 183, 184 

tetragona, 183 
Depluming scabies, 219 
Dermaglyphus elongatus, 220 

minor, 220 

varians, 220 
Dermanyssus gallinte, 214 
Dermestes lardarius, 214 
Diaphragm, 56 
Diarrhea, simple, 159 
Digits. 5 

Diphtheria, avian, 96 
Discolored yolks, 170 
Diseases of the alimentary tract, 154 

of the oviduct. 164 

of the peritoneal cavity, 172 

of the respiratorv tract, 162 
Disinfectants. 22, 23, 24 
Disinfecting buildings. 22 
Dispharagvis hamulosus, 178 

laticeps, 178 

nasutus, 178 

spiralis, 179 

imcinatus, 181 



SUBJECT INDEX 



329 



Distention of the bursa of Fabricus, 161 

Dithyridium variabile, 200 

Docophoriis icterodes, 29 

Double-yolked eggs, 171 

Drooping abdomen, 173 

Dropsy, 173 

Dubbing wattles, 298 

Duck cholera, 250 

Ducks, infectious diseases of, 242 

septicemia of, 249 
Duodenum, 12, 13 



E 



Echinococcus polymorphus, 194 
Echinorhynchus polymorphus, 193 
Echinostomum conoideum, 192 

echinatum, 192 

filicollis, 192 

recurvatum, 192 

spserocephalus, 192 
Edema of wattles, 41 
Egg, blood spots in, 169 

bound, 165 

double yolked, 171 

eating, 176 

soft shelled. 171 

structure of, 168 
Eimeria avium, 127 
Epsom salts, 160, 186 
Emphysema, cutaneous, 297 
Enteritis, 158 

Entero-hepatitis of turkeys, 120 
Eosinophiles, 8 
Epidermoptes bifurcatus, 220 

bilobatus, 220 
Episternal process, 3 
Epithelioma contagiosum, 96 
Epizootic dysentery of fowls and tur- 
keys, 43 

pneumo-pericarditis in the turkey, 
43 
Ergot, toxicity, 283 
Esophagus, parasites of, 178 
External parasites, 208 
Exudative septicemia of geese, 243 

F 

Falculifer anatina, 220 

anserina, 220 

cornutvis, 220 

rostratus, 203, 220 
Favus, 116 
Feathers. 17 
Feather cysts, 265 

pulling, 176 
Femur, 4 



Ferrous sulphate, toxicity, 283 
Filaria anatis, 203 

clava, 203 

cygni, 182 

mansoni, 201 

spicularia, 238 
Fimbriaria fasciolaris, 183 
Flagellates, 192 
Flea, bird, 212 
Flight, prevention of, 300 
Flukes, 192 

Foot and mouth disease, 142 
Foot mange, 218 
Formaldehyde gas, 22 
Formalin, 22 
Fowl cholera, 34 

fever, 135 

plague, 81 

tick, 221 

typhoid, 50 
Fractures of bones, 298 
Freyana chanayi, 220 
Frozen comb, 300 
Furculum, 3, 4 



G 



Gangrene of ovary, 75 

Gape worms, 195 

Gasoline, 211, 238 

Gastritis, 157 

Geese, infectious diseases of, 242 

Gefliigelpest, 81 

General diseases, 150 

Generative system, 16 

Gizzard, 12 

parasites of, 178 
Gonglyonema ingluvicola, 179 
Goniocotes abdominalis, 209 

chrysocephalus, 209 

compar, 209 

hologaster, 209 

rectangulatus, 209 
Goniodes colchicus, 209 

damicornis, 209 

dissimilis, 209 

falcicornis, 209 

minor, 209 

numidanus. 209 

parviceps, 209 

stvlifer, 209 

truncatus, 209 
Gout, 150 
Grouse disease, 62 

H 

Habits, vicious, 175 
Hsemomoeba danielewskyi, 203 



'« 



330 



SUBJECT INDEX 



Haemoproteus columbse, 203 

danielewskyi, 203 
Harvest mites, 217 
Heart, 6 
Hematozoa, 203 
Hemiclepsis tessellata, 195 
Hemorrhagic septicemia of fowls, 34 

of geese, 242 

of the ring dove, 45 

of the swan, 46 
Heterakis brasiliensis, 188 

columb£e, 188, 190, 194 

compar, 188 

compressa, 188 

differens, 188 

dispar, 188 

lineata, 188 

papulosa, 188 

perspicillum, 188 

vesicularis, 188 
Holostomum gracile, 192 

sphaerocephalum, 192 
Horn, cutaneous, 298 
Hiihnercholera, 34 
Hiihnerspirillose, 135 
Hiihner typhus, 50 
Humerus, 4 
Hymenolepis anatina, 183 

cantaniana, 183 

carioca, 183 

coronula, 183 

fasciata, 183 

gracilis, 183 

lanceolata. 183, 184 

megalops, 183 

meleagris, 183 

musculosa, 183 

parvula, 183 

setigera, 183 

sinuosa, 183 

tenuirostris, 183 
Hvpiene, 20 
Hystrichis cygni, 181 

elesans, 181 

tricolor, 181 



Heum, 13 

Ilium, 4 

Impaction of crop, 156 

Incision of crop, 300 

Incubating periods, 18 

Indigestion, 157 

in parrots. 158 
Infectious diseases of geese and duck 
242 

enteritis of pheasants, 47 



Infectious entero-hepatitia of turkeys, 
120 

necrosis of canaries, 252 
Inflammation of crop in pigeons, 156 

of the oviduct, 164 
Infraorbital sinuses, 14 
Internal parasites, 178 
Intestines, 12 
Ipecac, toxicity, 283 
Ischium, 4 



Jejunum, 13 



K 



Keel, 3 

Kerosene emulsion, 215 

oil, 213 
Kidneys, 16 
Killing poultry, 314 



Laminosioptes cysticola, 202 
Large mononuclear leucocytes, 8 
Larynx, 14 
Lead water, 295 
Leg weakness, 153 
Leiomyoma, 267 
Leucocytes, 7 
Leucocytozoa, 204 
Leucocytozoon anatis, 205 

infection in ducks. 205 

infection in ostrich, 239 

struthionis, 239 
Leukemia, 146 
Lice, 208 
Limberneck, 154 
Linseed oil, raw, 240 
Liotheum longicaudum, 209 
Lipeurus anatis, 209 

anseris. 209 

baculus, 209 

crassicornis, 209 

heterographus, 208 

meleagridis, 209 

numidae, 209 

temporalis, 209 

variabilis, 208, 209 
Liver, 14 

complaint, 88 

parasites of, 194 
Lophophvton gallinse, 116 
Limgs. 15 

cono-estion of, 162 
Lymphatics. 7 
Lymphocytes, 8 



SUBJECT INDEX 



331 



Lymphoma, 265 
Lympho sarcoma, 272 
Lynchia maura, 204, 213 
livicolor, 204 

M 

Macroblasts, 8 
Maladie du somneil, 30 
Malaria, avian, 203 
Male fern, toxicity, 285 
Malta fever, 143 
Manson's eye worm, 201 
Mast cells, 8 
Megninia cubitalis, 220 

columbse, 220 

ginglymura, 220 

velata. 220 
Megrims of pigeons, 57 
Menopon biseriatiim, 208, 209 

giganteum, 209 

longicephalum, 209 

niimidte, 209 

obscurum, 209 

pallidum, 208 

phaeostomum, 209 

productum, 209 
Mercurial ointment, 212 
Mercuric chloride, toxicity, 229 
Metroliaathes lucida, 183 
Metorchis xanthosomua, 194 
Microblasts, 8 
Micrococcus melitensis, 143 
Microlynchia persilla, 204 
Mites, 214 

in connective tissue, 202 
Monas anatis, 193 
Monocercomonas anatis, 193 
Mouth, 10 
]\Tuscular system, 5 
Myelogenous leucocytes, 9 
Myxo fibroma, 274 

sarcoma, 273 



N 



Nasal cavity, parasites of, 195 

Nervous system, 9 

Nest bugs, 214 

Nodular tapniasis, 185 

Nostrils, 14 

Notocotyle verrucosa, 192 



O 



Oidium albicans, 155 
Opisthorchis simulans. 194 
Ornithonomus cycni, 209 
Ornithomyia avicularia, 213 



Osteo arthritis in geese and ducks, 246 
Osteochondrosarcoma, 267 
Ostrich, caponizing, 311 

diseases of, 226 
Ovary, 16, 17 
Oviduct, 16 

diseases of, 164 
Oxyspirura mansoni, 201 



Palate, 1 

Pancreas, 12, 13 

Paralysis of the ostrich, 231 

of bursa of Fabricus, 194 
Parasites, external, 208 

internal, 178 

of nasal cavity, 195 
Parrot septicemia, 54 
Parrots, indigestion in, 158 
Pasteurella avium, 34 
Pasteurellosis avium, 34 
Patella, 4 

Pectoral muscles, 5 
Pelvic bone, 4 

Perchloride of iron, 297, 301 
Peritoneal cavity, diseases of, 172 
Peritonitis, 174 
Permanganate of potash, 105 
Peste aviaria, 81 
Petrol, 238 
Petroleum, crude, 216 
Phalanges, 5 

Pheasants, infectious enteritis in, 47 
Phenol, 23 

Philopterus cygni, 209 
Phosphorus, toxicity, 285 
Physaloptera truncata, 178 
Pip, 101, 154 

Plasmodium danielewskyi, 203 
Pneumo-mycosis, 111 
Pneumonia, 163 

brooder, 111 
Poisons, 276 

Polymorphonuclear leucocytes, 8 
Polyneuritis, 153 
Pomegranate root bark, 187 
Post-mortem examination, 25 
Potassium permanganate, 24, 72 

toxicity, 286 
Poultrv houses, 21 
Pox, bird. 96 
Prevention of flight, 300 
Prolapse of oviduct, 167 
Prosthogonimus cuneatus, 195 

japonicua. 195 

ovatus, 195 
in eggs. 169 

pellucidus, 179, 195 



s 



332 



SUBJECT INDEX 



Proven triculus, 12 

parasites of, 178 
Pseudo leukemia, 146 
Psittacosis of parrots, 54 
Pterolichus obtusus, 220 
Pterophagus strictus, 220 

uncinatus, 220 
Pubis, 4 

Pulex avium, 212 
Pulse rate, 18 
Pygostyle, 3 



Quail disease, 63 



Q 



R 



Rabies, 142 

Rachitis, 152 

Red blood corpuscles, 7 

Respiration frequency, 19 

Respiratory system, 14 

tract, diseases of, 162 
Rheumatism, 88 
Ribs, 3 

Ring dove, 45 
Rose chafers, toxicity, 287 
Roimd worms, 188 
Roup, 96 
Rump gland, 17 
Rupture of the oviduct, 165 



Saccharomyces albicans, 155 
Salicylic acid, 288 
Salmonellosis, avian, 59 
Sanitation, 20 
Santonin, toxicity, 288 
Sarcopsylla gallinacea, 213 
Sarcoptes Ispvis, 219 

mutans, 218 
Scaly leg, 218 
Scapula, 3 
Schlafkrankheit, 30 
Schlafsucht, 30 
Schleg's solution, 220 
Sclerostomum anseris, 181 
Septic enteritis of cross bills, 259 

fever of the canary, 252 
of the parrot, 54 
Septicemia of ducks, 249 

caused by colon bacilli, 61 
Shadow cells, 8 
Simple diarrhea, 159 
Skeleton, 1 
Skin, 17 
Skull, 1 



Sleeping disease, 30 

Small mononuclear leucocytes, 8 

Sodium chloride, toxicity, 289 

fluorid, 210 

nitrate, toxicity, 290 

salicylate, 197 
Soft-shelled eggs, 171 
Soil, relation to health, 20 
Soor, 155 
Spinal cord, 9 
Spindle cell sarcoma, 268 
Spirochseta anserina, 135 

gallinarum, 135 
Spirochetosis, 135 
Spiroptera emmerzii, 201 . 

pectinifera, 179 
Spotted liver, 88 
Spur, 5 
Staphylococcus pyogenes aureus, 232, 

246 
Sternostomum rhinolethrum, 195 
Sternum, 3 

Stomoxysis calcitrans, 99 
Streptococcus, 28 

capsulatus gallinarum, 31 
Strongylus douglasi, 233 

nodularis, ISO 

quadriradiatus, 190 

tenius, 188 
Strychnine sulphate, toxicity, 291 
Styptic collodion, 301 
Suborbital sinuses, 14 
Sulphur, flowers of, 211 

ointment, 219 

toxicity, 293 
Swan, hemorrhagic septicemia in, 46 
Syngamus bronchialis, 195 

trachealis, 195 
Svrinx, 15 



Taenia exilis, 183 

fasciolaris, 183 

struthionis, 237 
Taeniasis, 182 

Tapeworm of the ostrich, 237 
Tapeworms, 182 
Tarso-metatarsal bone. 5 
Tartar emetic, toxicity. 293 
Temperature, normal, 19 
Tenebrio molitor, 214 
Thrush. 155 

Thorn-headed worms, 192 
Thymol, 237 
Tibia, 4. 5 
Ticks. 221 

Tobacco, vermifuge, 189 
Toe pecking, 175 



SUBJECT INDEX 



333 



Toxicology, 276 
Trachea, 15 
Trematodes, 102 
Treponema gallinarum, 135 
Trichomastix eberthi, 193 

gallinarum, 103 
Trichomonas, 120 

cohimbse, 192 

eberthi, 192 

gallinarum, 193 

pullorum, 193 
Trichomoniasis, 193 
Trichosoma anatis, 188 

annulatum, 179 

candinflatum, 191 

collare, 191 

cohimbfe, 191 

contortum, 181 

dubium, 191 

gallinum, 191 

nodularis, 179 

retiisum, 190 

strumosum, 179 
Trichostrongylus douglasi, 233 

pergracilis, 63 
Trinoton anseris, 209 

litiiratum. 209 

luridum, 209 
Tropisurus fissipinus, 181 
Trypanosomiasis, 203 
Tuberculin, avian, 91 

test. 91 
Tuberculosis, avian, 88 
Tvimors, 261 
Turbinated bones, 14 



Turpentine, 186, 294 

U 

Ulna, 4 
Ureters, 16 
Urinary system, 16 
Uropygium, 17 



Veins, 7 
Vent gleet, 167 
Ventriculus bulbosus, 12 
Vertebrae, 1 
Vertebral column, 1 
Vicious habits, 175 
Visceral gout, 150 
Vitamines, 153 

W 

Wattles, 18 

Weisser Kamm, 116 

White blood corpuscles, 7 

White comb. 116 

White diarrhea, 68 

Whitewash, 24 

Wireworms in the ostrich, 233 

Wishbone, 3 

Wounds, 301 



Yolks, discolored, 170 



PRINTED IN THE UNITED STATES OF AMERICA 



'XHE following pages contain advertisements of a few of the 
Macmillan books on kindred subjects. 



s 



The Clinical Pathology of the 
Blood of Domesticated Animals 

By SAMUEL HOWARD BURNETT, A.B., M.S., D.V.M. 

Professor in Comparative Pathology, New York State Veterinary 

College, Cornell University, Ithaca, N. Y. 

III., Cloth, 8°, $2.25 
The purpose of this book is to furnish a text-book of hematology 
for the use of students and practitioners of veterinary medicine. It 
is also intended to render easily accessible for investigators data con- 
cerning the blood of the kinds of experimental animals commonly used. 

TABLE OF CONTENTS 

CHAPTER 

1. Methods of Examination. 

2. Morphology of the Formed Elements. 

3. Normal Blood of the Several Domesticated Animals. 

4. Variations in Red Corpuscles and Hemoglobin. 

5. Influences Affecting the Leucocytes. 

6. Special Diseases of the Blood. 

7. General and Infectious Diseases. 

8. Specific Infectious Diseases Due to Bacteria and Fungi. 

9. Infectious Diseases Due to Protozoa. 

ID. Diseases Whose Cause Has Not Been Definitely Determined. 
II. Diseases Due to Animal Parasites. 

A Text-Book of Parasitology: 

For Veterinary Students 

By benjamin M. UNDERHILL, V.M.D. 
Instructor in Zoology, Parasitology and Histology, University of Penn- 
sylvania School of Veterinary Medicine 

Preparing. 

This work, while designed primarily as a text and reference for students and 
practitioners in veterinary medicine, will be found a concentrated and handy 
reference book by practitioners of human medicine, students in zoologJ^ and 
laboratory workers. Heretofore veterinary students in this country have had 
to rely upon circular matter of this character or upon special chapters scattered 
in works of other titles. 

The work contains little that is historical or critical. Parasitic species un- 
common in this country, or pathogenically unimportant, are omitted, though 
such as are now regarded as rare, but which in the future may become numerous 
and important, are given warranted consideration. 

A feature of the work which marks a distinct advance in the text-book treat- 
ment of parasitology is the attention given to the biological side of parasitism. 
This is essential to the student for his proper conception of the whole subject, 
and is certainly a prerequisite to intelligently applied measures of parasitic 
control. 

The work fills a long felt want in our veterinary schools, and altogether, it 
is a valuable and much needed addition to our American veterinary literature. 



THE MACMILLAN COMPANY 

Publishers 64-66 Fifth Avenue New York 



S 



Practical Veterinary Pharmacology 
and Therapeutics 

By HOWARD JAY MILKS 
Professor of Therapeutics and Small Animal Clinic, New York State 

Veterinary College, Cornell University 

8vo. $4.25 

This book is designed as a text-book for students and practitioners in 
veterinary medicine. In addition to the usual discussion on the action 
and uses of drugs there are chapters on the method of action of drugs, 
incompatibilities, solubilities, prescription writing and biologic prepa- 
rations. 

Drugs are grouped according to their therapeutic indications or uses 
and the general therapeutic considerations are taken up just before the 
members of the group are discussed in detail. Thus the general ac- 
tions and uses of the group and the detailed study of the drugs belong- 
ing to it are discussed in the same chapter. This plan differs from 
many texts in which the various therapeutic groups are discussed 
briefly in the first part of the book and to which no reference is made 
under the detailed discussion of the drugs. 

The Diseases of Animals 

By nelson S. MAYO 

Cloth, Illustrated, i2mo, $1.75 

The author gives advice in a brief and popular manner on the dis- 
eases and ailments of farm animals. It is a book which will enable 
those who have the care of animals to detect indications of disease and 
to make timely application of the necessary remedies. 

" It includes about all that the practical keeper of live-stock has need 
of, and the method of presentation could hardly be better. The expo- 
sition has the charm of perfect clearness and simplicity, which makes 
the book agreeable even to the reader not in search of specific facts." — 
Country Gentleman. 



THE MACMILLAN COMPANY 

Publishers 64-66 Fifth Avenue New York 



The Pathology and Differential Diagnosis 
of Infectious Diseases of Animals 

By VERANUS ALVA MOORE, B.S., M.D., V.M.D. 

Professor of Comparative Pathology, Bacteriology and Meat Inspec- 
tion, and Director of the New York State Veterinary College, 
Cornell University, Ithaca, N. Y. 

Cloth, 8vo, III., $4.00 

This edition has been carefully revised, much of it rewritten and numerous 
additions made. It has been kept, however, within the limits of a text-book. 
Two appendices have been added, one on the requirements for interstate ship- 
ment of live stock and the other on the Federal regulations for the veterinary 
inspection of meat. These may be of much assistance to veterinarians. The 
diseases not indigenous to, or imported into, this country have been accorded 
much less space than those existing here. The desire is to emphasize the nature 
of the diseases our veterinarians are liable to encounter and, at the same time, 
give the characteristics of the others. The same plan of presenting the subject 
and of grouping the diseases according to their etiology, that was followed in 
the previous editions, has been retained in this. 

Principles of Microbiology: A Treatise 

on Bacteria Fungi and Protozoa Pathogenic 
for Domesticated Animals 

By VERANUS ALVA MOORE, B.S., M.D., V.M.D. 

Cloth, 8°, III., $4.00 

This volume has been prepared as a text-book for veterinary students begin- 
ning the study of microbiology. It is the outgrowth of a lecture course which 
has accompanied the laboratory work in bacteriology and protozoology. The 
author has endeavored to choose the material that will be of most help to the 
student of animal diseases and to avoid as much as possible matters of contro- 
versy. In its preparation, the purpose has been to point out the place and role 
of micro-organisms in nature; to give the methods for their study and identifi- 
cation; to indicate the relation of certain species to animal diseases; to give a 
description of the more important species pathogenic for animals; and a brief 
discussion of the reaction of the tissues to microbian invasion and the theories 
of immunity. In order that the volume be of further aid as a key to the entire 
subject, numerous references to the literature are given where the student can 
obtain at first hand the results of original research. 



THE MACMILLAN COMPANY 

Publishers 64-66 Fifth Avenue New York 



Medical and Veterinary Entomology 

By WILLIAM B. HERMS 

Associate Professor of Parasitology in the University of California; 

Consulting Parasitologist for the California State 

Board of Health, etc. 

Cloth, 8vo, illustrated, $4.00 

A work of interest to physicians, veterinarians, health officers, and 
sanitarians as well as to students. Herein is contained a discussion 
of all the more important insects and arachnids relating to disease and 
irritations of man and beast. The author has placed special emphasis 
on control and prevention. He has aimed to familiarize the student 
with the specific parasite treated in a chapter, its identity, life history, 
habits, relation to disease transmission or causation, and to indicate 
methods for its control and prevention. There are 228 illustrations in 
the text, largely made from original photographs or drawings. 



General Surgery 



By dr. EUGEN FRoHNER 

Professor in the Royal Veterinary College in Berlin 

Third Revised Edition 

Authorized Translation by D. HAMMOND UDALL, B.S.A., V.M.D. 

Professor of Medicine and Hygiene, N. Y. State Veterinary College, 

Ithaca; Major, Veterinary Reserve Corps, U. S. Army 

Cloth, 8°, $3.00 

The new third edition of general surgery is improved and enlarged 
in many respects. The chapter on etiology of tumors has been re- 
written, and many additions made. The chapter on botryomycosis has 
been newly written to harmonize with the most recent investigations 
on this subject. The chapter on tuberculosis has been retained and 
even enlarged. The important chapter on chronic deforming ar- 
thritis has been supplemented with the results of recent inve-^^-'^^ations 
made in D. Frohner's clinic upon ring-bones, chronic gonitis, and omar- 
thritis. Recent investigations on myositis, neuritis, healing of frac- 
tures, necrosis bacilli, pseudo-edema bacilli, and foal-lameness have also 
been considered. 



THE MACMILLAN COMPANY 

Publishers 64-66 Fifth Avenue New York 



LIBRARY OF 



CONGRESS 




-m-i^- 






.•■. ■ \f.v.'k^;;i.;,,-' 






m 



;.;(::;, 



^^^^i.:::^^ 



't''^ 


■vV 




'.', •>-' 


■• : ;■■ 


; -1 x-'-,;- ■ ■• -.V 


,', '!-': 


••V- 


;M>,V;.',-::|-,v 


:;-^' 








:'i 


':v-:,.:-^;;^ ■; 



.-:^l-^-. 






